Pharmaceutical composition for treating rheumatoid arthritis and preparation method thereof

Abstract

Provided are a pharmaceutical composition for treating rheumatic arthritis, and the use thereof in the preparation of a medicament for treating rheumatoid arthritis, an anti- inflammatory and analgesic medicament, a medicament for inhibiting an increase in capillary vessel permeability, and a medicament for inhibiting the proliferation of spleen lymphocytes and the production of serum type II collagen antibodies, reducing the content of inflammatory cytokines IL-1 and TNF-α, and inhibiting the production of rheumatoid factors IgG and IgM. The pharmaceutical composition is prepared from the following medicinal materials, in parts by weight: 120-190 parts of Radix Astragali, 120-190 parts of Radix Gentianae Macrophyllae, 45-80 parts of Radix Stephaniae Tetrandrae, 45-80 parts of Radix Aconiti Lateralis Preparata, 110-180 parts of Rhizoma et Radix Polygoni Cuspidati, 110-180 parts of Stem Caulis Spatholobi, 110-180 parts of Rhizoma et Radix Clematis, 20-40 parts of Semen Sinapis Albae, 45-80 parts of Radix Paeoniae Alba, 120-190 parts of Radix Rehmanniae Recens, 45-80 parts of Radix Angelicae Sinensis, 40-65 parts of Myrrha, 40-65 parts of Rhizoma Cyperi, 45-80 parts of Ramulus Cinnamomi and 45-80 parts of Radix Achyranthis Bidentatae.

Description

PHARMACETUTICAL COMPOSITION FOR TREATING RHEUMATOID ARTHRITIS AND PREPARATION METHOD THEREOF Technical field The present invention relates to a Chinese medicine composition for treating rheumatoid arthritis and a preparation method thereof. It belongs to the field of application of Chinese herbal medicine and is mainly used clinically for rheumatoid arthritis, and the symptoms thereof include swelling, pain and tenderness of limb joints, morning stiffness, difficulty in joint flexion and extension, limited movement of the joints, numbness and heaviness of limbs, subcutaneous nodules, fear of cold and wind, mental fatigue, etc. Background technology Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by erosive arthritis. The prevalence of the disease is 0.8% of the population (range 0.3% to 2.1%), and it is more frequent in females, who are about three times more likely to be affected than males. RA can occur at any age, with the peak incidence between 30 and 50 years old. According to a survey conducted by the Rheumatology Society of the Chinese Medical Association in Beijing and Guangzhou, the prevalence of RA was 0.34% in the north and 0.32% in the south. The main clinical manifestations of RA are symmetric and persistent joint swelling and pain, often accompanied by morning stiffness. The most affected joints are the proximal interphalangeal joints, metacarpophalangeal joints, wrists, elbows, and toe joints; at the same time, the cervical vertebrae, temporomandibular joints, and sternoclavicular and acromioclavicular joints can also be affected. In the middle and advanced stages of the disease, patients may develop "swan neck" and "button flower" deformities of the fingers, joint ankylosis and subluxation of the metacarpophalangeal joints, which is characterized by the metacarpophalangeal joints being deviated to the ulnar side. In addition to joint symptoms, subcutaneous nodules, called rheumatoid nodules, may be present; some patients may have a combination of extra-articular manifestations in the lungs, eyes, cardiovascular system and nervous system. The etiology of this disease is unknown and may be related to infection, genetics and other factors that induce autoimmunity, and its pathogenesis is complex. Studies have shown that RA is an autoimmune disease mediated by T cells, with the participation of macrophages, dendritic cells, B cells, and inflammatory cells, etc. The pathological manifestations of this disease are mainly chronic inflammation of synovial membrane of the joints, formation of vascular cataracts, and destruction of cartilage and bones of joints, which ultimately lead to deformity of the joints and loss of function. RA is extremely harmful, with a large group of patients and a high rate of disability, 60% for 5-10 years, 90% for 30 years, and the 5-year mortality rate with extra- articular manifestations can be as high as 50%, and it has become one of the main causes of labor force loss and disability in China. In addition, most of the patients do not receive effective and timely treatment, therefore, active research on the prevention and treatment of RA is urgently needed. The treatment of RA has been a difficult and hot spot in field of rheumatology for a long time. At present, the objectives of western medicine in treating this disease are to reduce or eliminate joint swelling, pain, morning stiffness or extra-articular symptoms caused by arthritis; to control the development of the disease, to prevent and minimize the destruction of the joints and bones, to achieve a longer period of clinical remission, and to maintain the function of the affected joints as much as possible; to promote the repair of the destroyed joints and bones and to improve their function; and at the same time to control the systemic involvement of the system, however, the medicines applied in the treatment of RA at present are regarded as palliative treatments aiming at relieving the clinical symptoms. Pharmacologic therapy for RA usually consists of five types: nonsteroidal anti-inflammatory drugs, disease- modifying anti-rheumatic medicaments, glucocorticoids, anticytokine agents, and immunomodulators. Among them, Ibuprofen, Naproxen, Indomethacin and Diclofenac are non-specific symptomatic medicaments, but these medicaments cannot prevent the development of the disease and comorbidities, and at the same time, there are some side effects such as: gastrointestinal irritation, azotemia, platelet dysfunction, allergic rhinitis, and exacerbation of asthma, etc., and interstitial damage of the kidneys can be seen after prolonged use of this kind of medicaments. Methotrexate, Salazosulfapyridine, Leflunomide, Penicillamine, Azathioprine, Cyclophosphamide, Cyclosporine, etc., most of the anti-rheumatic medicaments to improve the condition have adverse reactions such as hepatic and renal impairment, gastrointestinal reactions, bone marrow suppression, etc.; Glucocorticoids cannot prevent the destruction of the joint structure in the long term, and cannot improve the lesion development, and the long term application of the tolerated amount of increase, the difficulty of withdrawing, and the discontinuation of the medicament is likely to lead to the recurrence of the disease, accelerating the destruction of the joints. After regular internal medicine treatment, the patient's condition still cannot be controlled, in order to correct the deformity, improve the quality of life can be considered surgical treatment, commonly used surgery are synovectomy, artificial joint replacement, joint fusion, and soft tissue repair, but surgical treatment does not cure the disease and medication is still needed after surgery. In addition, autologous stem cell transplantation, T-cell vaccines, and mesenchymal stem cell therapy may be effective in the remission of RA, but only in a small number of patients and further clinical studies are needed. Therefore, the search for new therapeutic methods and measures, the development of highly effective and low-toxicity medicaments and effective and reasonable treatment programs are important measures to significantly improve patients' symptoms and reduce the incidence of disability caused by RA, and they are also cutting-edge topics that are generally emphasized by the medical community at home and abroad at present. Currently applied western medicaments for the treatment of RA mainly include anti- rheumatic for symptom improvement and anti-rheumatic for disease control. The latter group of medicaments is still in the exploratory and experimental stage, while the former group mainly includes non-steroidal anti-inflammatory drugs, disease-modifying anti-rheumatic drugs, biologics, and glucocorticoids. Nonsteroidal anti-inflammatory drugs (NSAIDs) have anti-inflammatory, analgesic, antipyretic, and joint swelling-reducing effects mainly through inhibition of cyclooxygenase (COX) activity and reduction of prostaglandin synthesis, and they are the most commonly used medicaments for RA treatment in the clinic; however, the presence of gastrointestinal symptoms, hepatic and renal impairments, and a possible increased number of cardiovascular adverse events have limited the use of the medicaments in patients with the aforementioned diseases, and even in the general population they require the use of the lowest effective dosage and a short course of treatment. Disease-modifying antirheumatic drugs (DMARDs), these drugs do not have significant pain-relieving and anti-inflammatory effects, so they are also known as slow-acting antirheumatic medicaments, but can slow or control the progression of the disease. Adverse effects such as gastrointestinal discomfort, hair loss, rash, liver and kidney damage, leukopenia, and bone marrow suppression are common with this class of medicaments. Clinically, early use is emphasized, and multi-drug combinations are required for more complex conditions with multiple joint involvement or extra-articular symptoms. Biological agents: mainly include tumor necrosis factor (TNF)-α antagonists: etanercept, infliximab, adalimumab; interleukin (IL)-l antagonists: anakinra; anti-CD20 monoclonal antibodies: rituximab; and T-cell co-stimulatory signaling inhibitors, etc. Because they are mostly administered subcutaneously or intravenously, they are associated with infections, infusion reactions, and adverse effects such as hypertension, rash, pruritus, fever, nausea, arthralgia, and drug-induced lupus-like syndrome and demyelinating lesions. Glucocorticoids: can rapidly improve joint swelling and pain and systemic symptoms. In severe RA with cardiac, pulmonary or neurological involvement, short-acting hormones can be given, and the dosage depends on the severity of the disease, but the application of hormones has the defects of difficulty in withdrawing the drug and easy recurrence of the disease after stopping the drug. Traditional Chinese medicine has conducted a lot of research on the identification and treatment of rheumatoid arthritis and has accumulated a wealth of experience, which is unique in reducing clinical symptoms, improving quality of life, and preventing / slowing down the development of complications, which makes up for the shortcomings of Western medicine and is increasingly being highly valued by both domestic and international medical communities. Currently, there are many kinds of Chinese patent medicines for the treatment of RA, with different specific effects and properties, including the following: drugs that dispel wind, remove dampness, warm meridians, and disperse cold, such as HanShiBi Granules, HanBiTing Tablets, Compound Snow Lotus Capsules, ZhuiFengTouGu pills, XiaoHuoLuo pills, etc.; drugs that nourish the liver and kidney, stimulate and activate the meridians, including FengShi HanTong Tablets, KuanBi Granules, ZhuangGuGuanjie Pills, YiShen JuanBi Pills, etc.; drugs that relax tendons, activate collaterals, activate blood circulation and relieve pain, including TongRen DaHuoLuo Pills, TongLuo KaiBi Tablets, DuHuo JiSheng Pills, PanLongqi Tablets, etc.; heat-clearing and damp-removing drugs, including ShiReBi Granules. In addition, there are single dosage extracted drugs such as Tripterygium wilfordii Polyglycoside Tablets and White Paeony Total Glycosides Capsules. Comprehensive analysis shows that most of the currently marketed RA Chinese patent medicine products are positioned in the aspects of dispelling wind and removing dampness, warming the meridians and dispersing cold, nourishing the liver and kidneys, stimulating and activating the meridians, relaxing the tendons, activating blood circulation and relieving pain, and clearing away heat and dampness. However, each type of medicine has its own focus, and there are not many drugs targeting the cause and onset of RA from the perspectives of wind, cold, dampness, heat, phlegm, blood stasis, deficiency, etc., and there is no way to understand the cause, pathogenesis and treatment of the disease from the theory of collateral disease. Summary The pharmaceutical composition of the present invention is an empirical formula for the treatment of rheumatoid arthritis, created by Prof. Yiling Wu, academician of the Chinese Academy of Engineering, vice president of the Chinese Society of Traditional Chinese Medicine, and vice president of the Chinese Society of Integrated Traditional Chinese and Western Medicine, honorary president of Hebei Yiling Hospital, according to the guidance by the theory of collaterals disease in Chinese medicine, from the comprehensive analysis of Chinese medicine pathogenesis and treatment of rheumatoid arthritis due to paralysis and obstruction of complex merdians caused by "wind, cold, dampness, heat, phlegm, stasis, and deficiency", and combined with many years of clinical experience in the treatment of rheumatoid arthritis, and clinically applied for nearly 20 years, with precise clinical efficacy. The pharmaceutical composition of the present invention is innovative in establishing prescription principles and formulating pharmaceutical compositions. First, the etiology and onset of the disease are comprehensively considered from multiple pathogenic factors such as wind, cold, dampness, heat, phlegm, stasis, deficiency, etc.; secondly, guided by the theory of collateral disease, it is proposed that deficiency of healthy Qi and invasion of collaterals by pathogenic Qi are the pathological basis of this disease, and the cementation of phlegm and blood stasis and obstruction of collaterals are the main disease links of this disease. Finally, it is proposed to dispel pathogenic Qi and relieve paralysis, replenishing Qi and dredging collaterals is the main treatment principle for this disease. The main treatment methods are dispelling wind, dispersing cold and removing dampness, replenishing Qi, removing blood stasis and dredging collaterals. The medicine is composed of Radix Astragali, Radix Gentianae Macrophyllae, Radix Stephaniae Tetrandrae, black Radix Aconiti Lateralis Preparata, Rhizoma et Radix Polygoni Cuspidati, Stem Caulis Spatholobi, Rhizoma et Radix Clematis, Semen Sinapis Albae, Radix Paeoniae Alba, Radix Rehmanniae Recens, Radix Angelicae Sinensis, vinegar fried Myrrha, Rhizoma Cyperi, Ramulus Cinnamomi and Sichuan Radix Achyranthis Bidentatae. With Radix Astragali and Radix Gentianae Macrophyllae as the sovereign drug, they can dispel wind, disperse cold, remove dampness, replenish Qi, dredge collaterals and relieve pain. At the same time, Radix Stephaniae Tetrandrae is used to strengthen the effect of removing dampness, dredging meridians and relieving pain, black Radix Aconiti Lateralis Preparata is used to warm the meridians, disperse cold and dredge meridians, Rhizoma et Radix Polygoni Cuspidati is used to clear away heat, diuresis and relieve pain, Stem Caulis Spatholobi is used to promoting blood circulation, remove blood stasis and dredge meridians, together, the ministerial drugs help the sovereign drug to dispel pathogenic Qi. It is supplemented with Rhizoma et Radix Clematis to dispel rheumatism, dredge meridians and numbness, Semen Sinapis Albae to clear away phlegm and dredge meridians, invigorate Qi and disperse stagnation, Radix Paeoniae Alba and Radix Rehmanniae Recens to nourish blood and nourish yin, Radix Angelicae Sinensis to nourish blood and dredge meridians, vinegar fried Myrrha to invigorate blood and dredge meridians and relieve pain, and Cyperi rhizome to regulate Qi and activates blood circulation. Ramulus Cinnamomi and Sichuan Radix Achyranthis Bidentatae are used as envoy drugs, which lead the medicines to reach the upper and lower joints, dredge meridians and remove paralysis. This medicine formulation comprehensively treats the internal and external causes of rheumatoid arthritis. It not only helps to improve patients' symptoms such as local swelling and pain in joints, stiffness in the morning, difficulty in flexion and extension, and limited movement, but also significantly improve systemic clinical symptoms such as numbress and weight in the limbs, chills and wind aversion, fatigue, and improve the patient's quality of life, demonstrating the unique advantages of this prescription. Compared with similar products, the pharmaceutical composition of the present invention is innovative in terms of etiology and pathogenesis, establishment of prescription principles and composition of prescriptions. Rheumatoid arthritis is caused by external factors such as wind, cold and dampness, which block the collaterals. In addition, on the basis of deficiency of healthy Qi, phlegm and blood stasis block the collaterals and form agglomerations. Doctors in the past dynasties have discussed this, such as "Su Wen Bi Lun", which proposed: "The three Qi of wind, cold and dampness come together and combine to cause paralysis"; "Jin Gui Yao Lue" records: "Pain in the limbs and joints, weakness in the body, and swollen feet as if they were falling off" should be treated with Ramulus Cinnamomi, Paeonia lactiflora and rhizoma anemarrhenae Decoction. Zhu Danxi's "Danxi Heart Method" points out: "The limb joint pain in obese people is mostly caused by rheumatism and phlegm flowing into the meridians." Ye Tianshi discussed in "Clinical Guidelines for Medical Records": "The three Qi of wind, cold, and dampness combine to cause numbness. However, over time, external pathogenic Qi remain, and both Qi and blood are injured. They turn into blood stasis and phlegm, which mixes with the meridians and causes various obstructions." Therefore, it is not difficult to find that the occurrence and development of this disease are related to various pathological factors such as wind, cold, dampness, heat, phlegm, blood stasis, deficiency, etc., and are closely related to collaterals. Throughout more than two thousand years of records on the etiology and pathogenesis of paralysis syndrome, the main aspects can be summarized as follows: (1) Insufficient healthy Qi: "Nei Jing" points out that "where evil comes, the Qi will be deficient" and "wind, rain, cold and heat cannot be deficient, and evil will not only hurt people." Insufficient healthy Qi plays a decisive role in the onset of paralysis. Insufficient healthy Qi mainly includes insufficient congenital endowment, old age, kidney deficiency, excessive work and rest, postpartum and illness, which can damage healthy Qi. As the "Zheng Zhi Zhun Sheng" says, "paralysis disease involves wind, dampness, cold, and heat... all symptoms, kidney deficiency is the radix cause." The kidney governs the bones. In the elderly, kidney deficiency, insufficient marrow, and loss of bone support may cause paralysis symptoms such as pain in the waist, spine, joints, and heels. At the same time, when the kidneys are deficient in the elderly, the healthy Qi is insufficient, the external defense is not solid, and the internal organs are empty, which makes it easy for wind, cold, dampness and other pathogenic Qi to invade the body and cause this disease. "People who are tired will have a lot of internal and external deficiency, weak blood and Qi, loose joints, easy invasion by wind and evil, and will suffer from numbness according to their feelings" ("Taiping Shenghui Prescription" by Wang Huaiyin of the Song Dynasty), pointing out that excessive fatigue can also lead to insufficient healthy Qi and failure to defend the outside world. Another example is that a woman's Qi and blood are greatly depleted after childbirth, and the healthy Qi is weakened. If the care is not taken properly, external pathogenic Qi such as wind, cold, and dampness can easily invade, which can also lead to the occurrence of paralysis. In addition, after the illness, the Qi is weak and unable to drive out the pathogenic Qi, causing the external pathogenic Qi to linger and stay in the blood vessels of the limbs, joints, muscles and bones for a long time, causing paralysis and blockage of the collaterals, making it difficult to heal. (2) Invasion of external pathogenic Qi: wind, cold, dampness and other external pathogenic Qi invade the body, and good and evil compete with each other. If the evils prevail and the good retreats, the disease will occur. Therefore, it is believed that external pathogenic Qi such as wind, cold, and dampness are the direct factors and objective conditions for the occurrence of this disease. Although a weak body can easily lead to the invasion of external pathogenic Qi, but the body is still good, but no attention is paid to nutrition, or the work is damp, eating and sleeping in the open air; or working in the water, wading in the rain; or living in a damp place, sleeping in the wind; or the weather changes suddenly, alternating between hot and cold; or sweating after exertion and wind, or showering with cold water after sweating, etc.; at this time, the external defense is relatively insufficient, external pathogenic Qi take the opportunity to attack the person, and change over time, wind, cold, and damp pathogenic Qi block the collaterals, leading to this occurrence of disease. Just as it is said in "Su Wen: The Generation of the Five Internal Organs": "When you lie down and the wind blows, the blood will condense on the skin and it will cause numbness." Zhang Zihe's "Ru Men Shi Qin " records: "This disease mostly occurs when it rains in four seasons. At that time... when the grass is dry and cold, or in places near water,... people who work hard are exposed to wind and rain, and the place where they sleep is damp, and the numbness comes in from the outside." (3) Phlegm coagulation and blood stasis: Phlegm turbid and blood stasis are not only pathological products produced by pathogenic factors acting on the body, but also can act on the body as a separate cause of the disease. As Yu Chang said in "Medical Law": The evils of the three paralysis diseases of wind, cold and dampness are supported by the phlegm in the chest." As the disease lasts for a long time, it affects the circulation of Qi and blood, causing blood stagnation to form blood stasis, body fluid to condense into phlegm, and phlegm and blood stasis to block each other, block the collaterals, and penetrate deep into the bones; or there are also external pathogenic Qi that cannot be resolved, internal and external pathogenic Qi are reconciled, and they are trapped and cemented in the collaterals, making the disease lingering and difficult to heal. Common symptoms in the late stage of the disease are obvious joint swelling and pain, difficulty in flexion and extension, limited movement, subcutaneous nodules, etc. As stated in "Introduction to Medicine": "The joints are extremely painful, and for a long time, the hands and feet will be curled up...and even the body will be lumpy." This is a sign of phlegm coagulation and blood stasis, and collateral obstruction and paralysis. "Long- term paralysis will lead to phlegm-dampness, blood stasis, and stagnant meridians" ("Syndrome-like Treatment: Treatment of Paralysis"). It can be seen that as time goes by, the circulation of Qi and blood will not be smooth, stop and cause blood stasis, and invaded by external pathogenic Qi, When the internal and external conditions are combined, the meridians are blocked, resulting in paralysis, and the body is weak due to long-term illness, making it difficult to remove pathogenic Qi and hard to heal from cementation. To sum up, doctors of past dynasties have recognized that the pathogenesis of paralysis is insufficient healthy Qi, external pathogenic Qi is invading, internal and external pathogenic Qi are combined, pathogenic Qi is blocked, or it is caused by phlegm turbid and blood stasis flowing into the muscles, joints, muscles and bones, poor circulation of Qi and blood, and obstruction of collaterals. The nature of the disease is a mixture of deficiency and excess. However, various schools of thought mostly understand the disease from one or two aspects such as deficiency, evil, phlegm, blood stasis, and heat, and there are few discussions on collateral diseases. However, the pathogenesis and symptoms of paralysis syndrome are complex, and the disease is prolonged and difficult to cure. The analysis of collateral disease comprehensively combines the multiple pathogenesis of "wind, cold, dampness, heat, phlegm, blood stasis, and deficiency" and has important clinical guiding value for comprehensively revealing the disease. In view of the above understanding, the inventor finds that rheumatoid arthritis is mainly characterized by joint swelling and pain, and its pathogenesis is due to deficiency of healthy Qi, external attack of wind, cold, and dampness, and phlegm and blood stasis condensing to block the collaterals. The occurrence and development of this disease is related to wind, cold, and dampness. It is related to various pathological factors such as cold, dampness, heat, phlegm, blood stasis, deficiency, etc., and is closely related to collaterals. Although the syndromes are differentiated by cold, heat, deficiency, and excess, the common disease feature is obstruction of Qi and blood in the collaterals of the body, fascia, and joints. Therefore, "dredging the collaterals" is the general treatment principle. The main treatment principles for this disease are dispelling evil and relieving paralysis, replenishing Qi and dredging collaterals. It is established that dispelling wind, dispersing cold and removing dampness, replenishing Qi, removing blood stasis and dredging collaterals are the main treatment principles for this disease. Doctors in the Ming and Qing Dynasties have elaborated on this. For example, Wu Jutong's "Wen Bing Tiao Bian" believes that "miscellaneous feelings are confused, and the disease is not one end, but the four words of Qi not controlling dredging as the key points." Therefore, it is emphasized that in the treatment of paralysis syndrome, "dredging is the first priority". Ye Tianshi pointed out in "Lin Zheng Zhi Nan Yi An Bi": "Despite the sweating, the symptoms are not relieved, it is important to dredging, as long as it is dredgeed, the retained evil can be expelled", in short, the evil will be eliminated if the Qi and blood are circulated, the camp and defense will return to normal, and the paralysis syndrome will be eliminated by the dredgeed collaterals. The inventor believes that based on the traditional Chinese medicine pathogenesis characteristics of rheumatoid arthritis caused by "wind, cold, dampness, heat, phlegm, blood stasis, and deficiency" leading to collateral obstruction, the treatment method is to "dispel wind, disperse cold and remove dampness, replenish Qi, remove blood stasis and dredge meridians", and use complex prescriptions to treat complex syndromes. Therefore, there are many types of medicines that make up the formula in this prescription, and the principle of the combination of two sovereign drugs and four ministerial drugs is used. The composition for treating rheumatoid arthritis according to the present invention comprises the following components by weight: 120-190 parts of Radix Astragali, 120-190 parts of Radix Gentianae Macrophyllae, 45-80 parts of Radix Stephaniae Tetrandrae, 45-80 parts of Radix Aconiti Lateralis Preparata, 110-180 parts of Rhizoma et Radix Polygoni Cuspidati, 110-180 parts of Stem Caulis Spatholobi, 110-180 parts of Rhizoma et Radix Clematis, 20-40 parts of Semen Sinapis Albae, 45-80 parts of Radix Paeoniae Alba, 120-190 parts of Radix Rehmanniae Recens, 45-80 parts of Radix Angelicae Sinensis, 40-65 parts of Myrrha, 40-65 parts of Rhizoma Cyperi, 45-80 parts of Ramulus Cinnamomi and 45-80 parts of Radix Achyranthis Bidentatae. The composition for treating rheumatoid arthritis according to the present invention comprises the following components by weight: 120 parts of Radix Astragali, 190 parts of Radix Gentianae Macrophyllae, 45 parts of Radix Stephaniae Tetrandrae, 80 parts of Radix Aconiti Lateralis Preparata, 110 parts of Rhizoma et Radix Polygoni Cuspidati, 180 parts of Stem Caulis Spatholobi, 110 parts of Rhizoma et Radix Clematis, 40 parts of Semen Sinapis Albae, 45 parts of Radix Paeoniae Alba, 190 parts of Radix Rehmanniae Recens, 45 parts of Radix Angelicae Sinensis, 65 parts of Myrrha, 40 parts of Rhizoma Cyperi, 80 parts of Ramulus Cinnamomi and 45 parts of Radix Achyranthis Bidentatae. The composition for treating rheumatoid arthritis according to the present invention comprises the following components by weight: 150 parts of Radix Astragali, 160 parts of Radix Gentianae Macrophyllae, 60 parts of Radix Stephaniae Tetrandrae, 65 parts of Radix Aconiti Lateralis Preparata, 120 parts of Rhizoma et Radix Polygoni Cuspidati, 130 parts of Stem Caulis Spatholobi, 135 parts of Rhizoma et Radix Clematis, 35 parts of Semen Sinapis Albae, 50 parts of Radix Paeoniae Alba, 160 parts of Radix Rehmanniae Recens, 60 parts of Radix Angelicae Sinensis, 55 parts of Myrrha, 45 parts of Rhizoma Cyperi, 60 parts of Ramulus Cinnamomi and 60 parts of Radix Achyranthis Bidentatae. The composition for treating rheumatoid arthritis according to the present invention comprises the following components by weight: 146 parts of Radix Astragali, 139 parts of Radix Gentianae Macrophyllae, 58 parts of Radix Stephaniae Tetrandrae, 75 parts of Radix Aconiti Lateralis Preparata, 120 parts of Rhizoma et Radix Polygoni Cuspidati, 125 parts of Stem Caulis Spatholobi, 135 parts of Rhizoma et Radix Clematis, 28 parts of Semen Sinapis Albae, 60 parts of Radix Paeoniae Alba, 150 parts of Radix Rehmanniae Recens, 70 parts of Radix Angelicae Sinensis, 60 parts of Myrrha, 60 parts of Rhizoma Cyperi, 70 parts of Ramulus Cinnamomi and 70 parts of Radix Achyranthis Bidentatae. The composition for treating rheumatoid arthritis according to the present invention comprises the following components by weight: 156 parts of Radix Astragali, 156 parts of Radix Gentianae Macrophyllae, 63 parts of Radix Stephaniae Tetrandrae, 63 parts of Radix Aconiti Lateralis Preparata, 146 parts of Rhizoma et Radix Polygoni Cuspidati, 146 parts of Stem Caulis Spatholobi, 146 parts of Rhizoma et Radix Clematis, 31 parts of Semen Sinapis Albae, 63 parts of Radix Paeoniae Alba, 156 parts of Radix Rehmanniae Recens, 63 parts of Radix Angelicae Sinensis, 52 parts of Myrrha, 52 parts of Rhizoma Cyperi, 63 parts of Ramulus Cinnamomi and 63 parts of Radix Achyranthis Bidentatae. In the components of the composition for treating rheumatoid arthritis according to the present invention, the Radix Aconiti Lateralis Preparata is preferably black Radix Aconiti Lateralis Preparata, the Myrrha is preferably vinegar fried Myrrha, and the Radix Achyranthis Bidentatae is preferably Sichuan Radix Achyranthis Bidentatae. The formulation dosage forms of the compositions according to the present invention may be a capsule, a tablet, a pill, an oral liquid, a granule or a powder. The active component of the pharmaceutical composition according to the present invention is made by the steps of: A. crushing Radix Stephaniae Tetrandrae into fine powder, 60 parts thereof being subjected to sterilizing by o-γ radiation, for later use; B. adding 5-8 times amount of water to Ramulus Cinnamomi, vinegar fried Myrrha, Rhizoma Cyperi, conducting continuous extraction of volatile oil for 5-10 hours by water vapor distillation method, collecting the volatile oil, filtering aqueous solution after distillation and collecting it into another container, for later use; C. adding 8-12 times amount of 50-80% ethanol to Radix Gentianae Macrophyllae, Stem Caulis Spatholobi, Radix Angelicae Sinensis, Semen Sinapis Albae, Radix Paeoniae Alba, and Rhizoma et Radix Polygoni Cuspidati, reflux extracting 1-3 times for 1 hour each time, filtering the extract, recovering ethanol under reduced pressure, concentrating them to a clear paste with a relative density of <com:Math><semantics>1.15±0.05<annotation encoding="application / x-tex">1.15 \pm 0.05< / annotation>< / semantics>< / com:Math>, for later use; D. adding 8-12 times amount of water to Radix Astragali, black Radix Aconiti Lateralis Preparata, Rhizoma et Radix Clematis, Radix Rehmanniae Recens, and Sichuan Radix Achyranthis Bidentatae, decocting 2-5 times with 1.5 hours each time, filtering decoction solution, and concentrating it under reduced pressure to a clear paste with a relative density of 1.10±0.05, combining it with a water solution after volatile oil distillation, concentrating it under reduced pressure to a clear paste with a relative density of 1.15±0.05, for later use; E. combining the clear paste prepared in steps C and D, mixing, drying, and crushing them to obtain mixed clear paste powder; the fine powder obtained in step A, the volatile oil obtained in step B, and the clear paste powder obtained in step E together constitute the active component of the pharmaceutical composition of the present invention. A process for preparation of the capsule in the pharmaceutical composition formulation according to the present invention comprises: A. crushing Radix Stephaniae Tetrandrae into fine powder, 60 parts thereof being subjected to sterilizing by o-γ radiation, for later use; B. adding 8 times amount of water to Ramulus Cinnamomi, vinegar fried Myrrha, Rhizoma Cyperi, conducting continuous extraction of volatile oil for 10 hours by water vapor distillation method, collecting the volatile oil, filtering aqueous solution after distillation and collecting it into another container, for later use; C. adding 10 times amount of 70% ethanol to Radix Gentianae Macrophyllae, Stem Caulis Spatholobi, Radix Angelicae Sinensis, Semen Sinapis Albae, Radix Paeoniae Alba, and Rhizoma et Radix Polygoni Cuspidati, reflux extracting 3 times for 1 hour each time, filtering the extract, recovering ethanol under reduced pressure, concentrating them to a clear paste with a relative density of <com:Math><semantics>1.15±0.05<annotation encoding="application / x-tex">1.15 \pm 0.05< / annotation>< / semantics>< / com:Math>, for later use; D. adding 8 times amount of water to Radix Astragali, black Radix Aconiti Lateralis Preparata, Rhizoma et Radix Clematis, Radix Rehmanniae Recens, and Sichuan Radix Achyranthis Bidentatae, decocting 4 times with 1.5 hours each time, filtering decoction solution, and concentrating it under reduced pressure to a clear paste with a relative density of 1.10±0.05, combining it with a water solution after volatile oil distillation, concentrating it under reduced pressure to a clear paste with a relative density of 1.15±0.05, for later use; E. combining the clear paste prepared in steps C and D, mixing, drying, and crushing them to obtain mixed clear paste powder; spraying the volatile oil obtained in step B, adding the sterilized powder obtained in step A, conducting spray granulation, rectification of the granules and capsulation. A process for preparation of the tablet in the pharmaceutical composition formulation according to the present invention comprises: A. crushing Radix Stephaniae Tetrandrae into fine powder, 60 parts thereof being subjected to sterilizing by o-y radiation, for later use; B. adding 6 times amount of water to Ramulus Cinnamomi, vinegar fried Myrrha, Rhizoma Cyperi, conducting continuous extraction of volatile oil for 8 hours by water vapor distillation method, collecting the volatile oil, filtering aqueous solution after distillation and collecting it into another container, for later use; C. adding 10 times amount of 70% ethanol to Radix Gentianae Macrophyllae, Stem Caulis Spatholobi, Radix Angelicae Sinensis, Semen Sinapis Albae, Radix Paeoniae Alba, and Rhizoma et Radix Polygoni Cuspidati, reflux extracting 3 times for 1 hour each time, filtering the extract, recovering ethanol under reduced pressure, concentrating them to a clear paste with a relative density of <com:Math><semantics>1.15±0.05<annotation encoding="application / x-tex">1.15 \pm 0.05< / annotation>< / semantics>< / com:Math>, for later use; D. adding 11 times amount of water to Radix Astragali, black Radix Aconiti Lateralis Preparata, Rhizoma et Radix Clematis, Radix Rehmanniae Recens, and Sichuan Radix Achyranthis Bidentatae, decocting 3 times with 1.5 hours each time, filtering decoction solution, and concentrating it under reduced pressure to a clear paste with a relative density of 1.10±0.05, combining it with a water solution after volatile oil distillation, concentrating it under reduced pressure to a clear paste with a relative density of 1.15±0.05, for later use; E. combining the clear paste prepared in steps C and D, mixing, drying, and crushing them to obtain mixed clear paste powder; F. conducting inclusion of the volatile oil obtained in step B to obtain an inclusion compound, for later use; G. granulating the sterilized powder obtained in step A with the clear paste powder obtained in step E, rectifying the granules, adding the inclusion compound obtained from step F, and pressing into tablets according to the conventional method. The process of volatile oil inclusion in the pharmaceutical composition of the present invention is as follows: taking 6-10 times amount of cyclodextrin of volatile oil, adding 6-10 times amount of water of cyclodextrin, carrying out grinding, then adding a mixture of the volatile oil and 90-95% ethanol in equal volume, continuing to grind evenly, and then drying to obtain the product. Preferably, the present invention also relates to use of the pharmaceutical composition according to the present invention in preparation of an anti-inflammatory drug. Preferably, the present invention also relates to use of the pharmaceutical composition according to the present invention in preparation of a drug for inhibiting increased capillary vessel permeability. Preferably, the present invention also relates to use of the pharmaceutical composition according to the present invention in preparation of an analgesic drug. Preferably, the present invention also relates to use of the pharmaceutical composition according to the present invention in preparation of a drug for inhibiting proliferation of splenic lymphocytes and production of serum antibodies to collagen type II, reducing contents of inflammatory cytokines IL-1 and TNF-<com:Math><semantics>α<annotation encoding="application / x-tex">\alpha< / annotation>< / semantics>< / com:Math>, and inhibiting production of rheumatoid factors IgG and IgM. Preferably, the rheumatoid arthritis treated by the pharmaceutical compositions of the present invention is preferably adjuvant arthritis or type II collagen-induced arthritis. In the pharmaceutical compositions of the present invention, the specific pharmaceutical compositions are: sovereign drugs: Radix Astragali and Radix Gentianae Macrophyllae. Radix Astragali: sweet and slightly warm, work specializing in tonifying Qi, is the holy medicine of tonifying Qi, in the internal can be used to tonify the Qi of the lungs and spleen, in the external can be solid surface and guard, as "Ben Cao Hui Yan" states, "Radix Astragali, tonifying the lungs and strengthening the spleen, strengthen the defense and reducing sweating, is a drug for driving the wind and transporting the poison"; "Ben Cao Zheng Yi" records: "(Radix Astragali) its skin taste thick, the power are in the skin, so it can reach the surface of the human skin muscle, strength the defense and protect Yang, enrich the surface, which is its specialty." This medicine is thin in Qi but strong in flavor, which can tonify the San Jiao and solidify the defense, and enrich the skin, so it is most suitable to be used as the Monarch to tonify the Qi of the lungs and spleen internally, and to benefit the Qi to strengthen the surface in order to prevent external pathogenic Qi from invading the body. Radix Gentianae Macrophyllae: pungent, sweet and flat in nature, dispelling wind and dampness, dispersing cold and relaxing the tendons, activating collaterals and relieving pain. "Ben Cao Jing Shu" says: "Radix Gentianae Macrophyllae, bitter can drain, pungent can disperse, slightly warm can facilitate, therefore, it treats cold and heat pathogenic Qi, cold-dampness and wind paralysis, limb and joint pain, and urination." Its properties include dispelling wind and removing dampness." Radix Gentianae Macrophyllae dispels wind and removes dampness, and is combined with Radix Astragali to replenish Qi and dispel evil, which can dispel evil without damaging the healthy Qi. And, Radix Astragali and Radix Gentianae Macrophyllae can replenish Qi without retaining evil. They have internal support mutually and can prevent external pathogenic Qi from coming back. The two medicines are used together to replenish Qi, dispel wind, remove dampness and disperse cold, dredge meridians and relieve pain, so they are used as sovereign drugs. Ministerial drugs: Radix Stephaniae Tetrandrae, black Radix Aconiti Lateralis Preparata, Rhizoma et Radix Polygoni Cuspidati, Stem Caulis Spatholobi. Radix Stephaniae Tetrandrae: bitter in taste and cold in nature, good at removing dampness, dredging meridians and relieving pain. "Treatise on the Properties of Medicine" states that it: "cures damp wind, mouth and face distortion, pain in the hands and feet, disperses phlegm", and helps Radix Astragali to strengthen the effect of removing dampness. Black Radix Aconiti Lateralis Preparata: pungent and sweet in taste and hot in nature, which is pungent and warm, dredges collaterals, warms the meridians and dispels cold. Radix Aconiti Lateralis Preparata is warm in nature and travel throughout the body without staying, it can be used to warm the meridians, disperse cold, remove dampness and relieve pain. It has the effects of dispelling wind and dampness, dispersing cold and relieving pain. "Ben Cao Hui Yan" calls it "a powerful medicine that restores yang energy, disperses yin and cold, expels cold phlegm, and clears joints." Zhang Xichun believes: "Radix Aconiti Lateralis Preparata has a pungent taste...its power can rise and fall, can reach internally and disperse externally. All the cold and cold knots in the organs and meridians and blood vessels can be opened and dredgeed", and it helps various medicines to clear collaterals, relieve numbness and dispel cold. Rhizoma et Radix Polygoni Cuspidati: slightly bitter in taste and slightly cold in nature, disperse blood stasis and relieves pain, dispels wind and dredges collaterals, clears away heat and removes dampness. "Ben Cao Shi Yi" states that "mainly for the wind between the joints and blood stasis". It is used in the prescription to clear blood stasis and heat, and is used to treat the syndrome of paralysis that accumulates for a long time and turns into heat. Stem Caulis Spatholobi: bitter and sweet in taste, warm in nature, promoting blood circulation and dredging collaterals, relaxing muscles and activating collaterals. "Yin Pian Xin Can" states that it can "remove blood stasis, generate new blood, and smooth the meridians." It is said to nourish blood and strengthen the body, remove blood stasis and dredge the meridians. The above-mentioned four medicines are used together with cold and warm to remove dampness and disperse cold, clear away heat and dampness, activate blood circulation and dredge meridians, and jointly contribute to the effect of the sovereign drugs in dispersing pathogenic Qi. Adjuvant drugs: Rhizoma et Radix Clematis, Semen Sinapis Albae, Radix Paeoniae Alba, Radix Rehmanniae Recens, Radix Angelicae Sinensis, vinegar fried Myrrha, Cyperi rhizome. Rhizoma et Radix Clematis: pungent and salty in taste, warm in nature, effective in dispelling wind and removing dampness, dredging collaterals and relieving pain. Clematis can dispel wind and damper, dredge meridians, and relieve arthralgia pain. It is an important medicine for treating arthralgia syndrome and muscle spasm. "Ben Cao Jing Shu" says: " Rhizoma et Radix Clematis is mainly for all winds, and it is a wind medicine that is suitable for guiding those medicines travelling throught the body." It is used to assist Radix Gentianae Macrophyllae and Radix Stephaniae Tetrandrae to enhance the effect of dispelling wind and removing dampness, taking advantage of its good traveling properties, and dredging meridians and relieving paralysis. Semen Sinapis Albae: pungent in taste and warm in nature, it can remove internal and external phlegm knots, expel phlegm and dredge meridians, promote Qi and disperse stagnation, and can treat phlegm-dampness, swelling, pain and numbness in limbs. "Ben Cao Qiu Zhen" says: "the pungent energy can enter the lungs, and the warmth can disperse the surface, the phlegm is in the skin and outside the membrane under the hypochondriac, this pungent warmth can be used as a tool for searching and eliminating, so that the inside and outside can be communicated without the risk of obstruction and stagnation." "Ben Cao Gang Mu" states that it: "invigorates Qi and removes phlegm, removes cold and warm, disperses swelling and relieves pain, cures asthma, cough, nausea, numbness, athlete's foot, and various pains in the muscles, bones, and waist joints." At the same time, this medicine warms the body and disperses cold, and assists Radix Aconiti Lateralis Preparata to strengthen the effect of dispersing cold. Radix Paeoniae Alba: bitter and acidic in taste and cool in nature, having a function of nourishing blood and dredging meridians, relieving pain. "Shen Nong Ben Cao Jing" says that it "removes blood paralysis", and "Bie Lu" says that it "dredges blood vessels". Radix Rehmanniae Recens: sweet in taste and cold in nature, nourishes blood and nourishes yin, dredges blood vessels and relieves blood numbness. Its effect of nourishing yin can also be used as an adjunct to the warming properties of black Radix Aconiti Lateralis Preparata, Stem Caulis Spatholobi, etc., and it can nourish and activate blood circulation together with Radix Paeoniae Alba, dispel the syndrome of blood stasis caused by arthralgia. Radix Angelicae Sinensis: sweet and pungent in taste and warm in nature. To treat wind, it first cures the blood, and the circulation of blood and wind will be eliminated. It has the function of nourishing blood, activating blood circulation and dredging meridians. "Ben Cao Zheng Yi": " Radix Angelicae Sinensis has a sweet and heavy taste, so it can nourish blood. Its Qi is light and pungent, so it can also promote blood circulation. It has action in the tonic and tonic in the action. It is a Qi medicine in the blood and also a holy medicine in blood... is used as an aid to clear the way, so it can relieve pain, relieve constipation, and sharpen the muscles and bones." Together with Stem Caulis Spatholobi and Radix Rehmanniae Recens, it also contains the meaning that to treat wind, blood must be treated first, and if blood circulates, wind will destroy itself. vinegar fried Myrrha: bitter in taste and neutral in nature, promotes blood circulation, dredges meridians and relieves pain. "Ben Cao Shu": "Taking it for a long time relaxes the fascia and dredges the blood vessels." "Ben Cao Yan Yi": "Myrrha may relieve stagnant blood." Cyperi rhizome: pungent and slightly sweet taste, neutral in nature, functions in promoting Qi and relieving depression, regulating Qi and relieving pain. Qi is the leader of blood, and when Qi moves, blood moves. Cyperi rhizome moves Qi to activate blood circulation, and together with Myrrha, it regulates Qi, activates blood circulation, and dredges collaterals. Envoy Drugs: Ramulus Cinnamomi and Sichuan Radix Achyranthis Bidentatae. Ramulus Cinnamomi: Pungent and sweet in taste and warm in nature, pungent and warm in unlock collaterals, and it can strengthen the effect of warming collaterals and dredging meridians. As stated in "Ben Jing Shu Zheng": "Ramulus Cinnamomi can benefit the joints, warm collaterals and dredge meridians, and this is it nature." At the same time, it can dispel wind and cold, and expel superficial pathogenic Qi. "ChangSha Yao Jie" states that it is good to dispel wind, best in adjusting wood Qi Shu, sooth the contractures of the tendons and veins, relieve the congestion of the joints. .....through the meridians and open paralysis, even to remove the dampness and cold". It is used as an envoy in the prescription, and leads the medicine upward. Sichuan Radix Achyranthis Bidentatae: sweet and slightly bitter in taste, flat in nature, and has the functions of dispelling wind and dampness, clearing joints, activating blood circulation and dredging meridians, and relieving muscle and bone pain. "Ben Jing" states that it "mainly treats cold-damp paralysis, spasm of limbs, and knee pain that cannot be bent." It is used as an envoy in the prescription, and leads the medicine downward. The two drugs are used together to induce the medicines to reach the upper and lower joints and dredge the meridians to relieve numbness and pain, so they are called envoy drugs. All medicines are used together, integrating cold and warmth into one body, smelting and replenishing them in one pot, integrating dispelling wind, dispersing cold, dehumidification, clearing away heat, replenishing Qi, activating blood circulation, eliminating phlegm, dredging collaterals and other products in the same prescription, aiming to "remove evil and relieve" paralysis, replenish Qi and dredge collaterals". In this way, the pathogenic Qi of wind, cold, dampness, phlegm, blood stasis and heat can be dispersed, the healthy Qi can be restored, the phlegm and blood stasis can be removed, the numbness and obstruction can be relieved, the collaterals can be dredgeed, and the Qi and blood can flow smoothly, then the disease will naturally heal. The pharmaceutical composition of the present invention has the effects of dispelling wind, dispersing cold and removing dampness, replenishing Qi, removing blood stasis and dredging meridians. It mainly treats rheumatoid arthritis with wind-cold-dampness syndrome, Qi deficiency, collateral stasis, and phlegm stasis. Traditional decoctions are troublesome to prepare, have poor taste and unstable quality, are inconvenient for patients to carry and take, and are greatly restricted in use. Therefore, it will be made into capsules, tablets, granules, oral liquid or other dosage forms. Among them, tablets use less excipients than other dosage forms, are easier to shape, are small in size, have accurate dosage, and are more convenient to carry, transport and take. In addition, tablets are dry solids with stable and controllable quality. Some drugs that are prone to oxidative deterioration and deliquescence can be protected by coating. Light, air, moisture, etc. have less impact on them, and can also cover up the bad smell of traditional Chinese medicine. Furthermore, tablet production is highly mechanized and automated, making it suitable for industrial promotion. In order to better leverage the social and economic value of the drug, we combined the properties of the prescription traditional Chinese medicine and preferred tablets as the dosage form of this prescription. During the research process of the preparation process, we started from many aspects and completed the process selection. First, we conducted a separate study on the medicinal properties of the composition. Radix Astragali mainly contains triterpene saponins, flavonoids, polysaccharides and other components. Modern research shows that Radix Astragali decoction has obvious tonic effects, and saponins, flavonoids, and polysaccharides are all active ingredients and are easily soluble in hot water, so it is appropriate to use the water decoction method. Radix Gentianae Macrophyllae mainly contains iridoid glycosides such as gentiopicroside and dangyaoside. The iridoid glycosides are easily soluble in solutions such as water or ethanol, and the ethanol extract of Radix Gentianae Macrophyllae has obvious anti- inflammatory effects. Based on the results of the solvent investigation, 70% ethanol was used for extraction. Radix Stephaniae Tetrandrae mainly contains tetrahydroisoquinoline alkaloids such as tetrandrine, Radix Stephaniae Tetrandrae Norin alkaloids, and cyclanoline. Radix Stephaniae Tetrandrae alkaloids have analgesic and anti-inflammatory effects, are not easily soluble in water, and are easily soluble in organic solvents such as ethanol. Combined with the results of solvent inspections, it can be easily extracted with alcohol. However, considering that the Radix Paeoniae Alba and Rhizoma et Radix Polygoni Cuspidati in the ethanol extraction part contain a large amount of tannins, anthraquinones and other ingredients, they are easy to precipitate with alkaloids and be lost. After experimental investigation, Radix Stephaniae Tetrandrae is easy to crush, and the fine powder is used as an excipient, and the preparation molding effect is better; because the proportion of Radix Stephaniae Tetrandrae in the formula is small, feeding after crushing will not lead to excessive dosage; at the same time, Crushing Radix Stephaniae Tetrandrae into medicine not only retains its active ingredients, but also reduces the amount of auxiliary materials used in preparation molding, which is more convenient for patients to take. Therefore, in this prescription, it is appropriate to crush Radix Stephaniae Tetrandrae into medicine. Radix Aconiti Lateralis Preparata mainly contains diterpene diester alkaloids. Radix Aconiti Lateralis Preparata decoction has an inhibitory effect on various animal models of acute and chronic inflammation, so it is appropriate to use water decoction. Stem Caulis Spatholobi mainly contains isoflavones, flavonoids, triterpenes and sterols, which are mainly alcohol-soluble components, extracted with 70% ethanol. Radix Angelicae Sinensis mainly contains volatile oils, organic acids, and polysaccharides. Modern research shows that the volatile oil in Radix Angelicae Sinensis has the effect of inhibiting the contraction of uterine smooth muscle. Currently, the volatile oil in Radix Angelicae Sinensis is mainly used for the treatment of dysmenorrhea and irregular menstruation. The main function of Radix Angelicae Sinensis in this prescription is to promote blood circulation, and the ferulic acid contained in it has the effects of inhibiting platelet aggregation and anti-thrombosis, and is the main component of promoting blood circulation. Based on the results of solvent inspection, 70% ethanol is used to extract it. Rhizoma et Radix Clematis mainly contains oleanane-type triterpenoid saponins. Saponins are easily soluble in water, so the decoction method is appropriate. Semen Sinapis Albae mainly contain various isothiocyanates such as mustardine and their glycosides, fatty acids, nitrogen-containing compounds and amino acids. Modern research shows that sinapine thiocyanate has anti-inflammatory effects and has a high extraction rate in ethanol. Combined with the results of the solvent investigation, 70% ethanol was used for extraction. Radix Rehmanniae Recens mainly contains iridoid glycosides, polysaccharides and other components. It is easily soluble in water, so it is better to use the water decoction method. Radix Paeoniae Alba mainly contains paeoniflorin, hydroxypaeoniflorin, benzoylpaeoniflorin and other glycosides and tannins. Paeoniflorin has the effects of inhibiting platelet aggregation, analgesia, and anti-inflammatory, and has a high extraction rate in ethanol. Based on the results of solvent inspection, 70% ethanol was used for extraction. Myrrha mainly contains volatile oil, resin and gum. Myrrha in the prescription is used to activate blood circulation and relieve pain. Modern research shows that both Myrrha volatile oil and water decoction have the effect of prolonging the coagulation time. Myrrha volatile oil has anti-inflammatory effects, therefore, the steam distillation method is used to extract, collect the volatile oil, and combine the aqueous solution and the decoction after distillation. Cyperi rhizome mainly contains volatile oil, which mainly contains sesquiterpenes and their oxides such as <com:Math><semantics>α<annotation encoding="application / x-tex">\alpha< / annotation>< / semantics>< / com:Math>-cyperoneone. Volatile oil and water decoction have analgesic effects, so they are extracted by steam distillation. The volatile oil is collected, and the aqueous solution and water decoction are combined after distillation. Rhizoma et Radix Polygoni Cuspidati mainly contains polydatin, anthraquinone, tannins and other ingredients. Polydatin and anthraquinone components have a higher extraction rate in ethanol. Based on the results of solvent inspection, 70% ethanol was used for extraction. Ramulus Cinnamomi mainly contains volatile oil and water-soluble components such as trans-cinnamic acid, protocatechuic acid, etc. The main component in the oil is cinnamic aldehyde, which has anti-inflammatory effects. Ramulus Cinnamomi combined with Radix Astragali decoction can significantly enhance the anti-inflammatory and analgesic effects of Radix Astragali. Therefore, the steam distillation method is used to extract, collect the volatile oil, and combine the aqueous solution and the decoction after distillation. Sichuan Radix Achyranthis Bidentatae mainly contains sterols. The decoction can significantly improve microcirculation and anti-inflammatory effects. Therefore, it is appropriate to use the water decoction method. For the volatile oil extraction in the prescription, the following investigations are performed: 1. Investigation on the extraction of volatile oil from Ramulus Cinnamomi: weighed 3 portions of Ramulus Cinnamomi sliced pieces, 200 g each for one portion, added 8 times the amount of water, extracted the volatile oil by steam distillation, recorded the volume of volatile oil every hour, and observed the oil production. Oil output: light yellow light oil, layered slowly, accompanied by white emulsion steaming out. The average oil yield was 0.79%. The volatile oil no longer increased after 6 hours of extraction, indicating that the extraction was basically complete. 2. Investigation on the extraction of Cyperi rhizome volatile oil: took an appropriate amount of Cyperi rhizome sliced pieces and coarsely chopped them into 3-5 mm particles and particles below 3 mm. Weighed 200g of Cyperi rhizome pieces, 3-5 mm particles and 3 mm or less particles respectively, made three parallel portions each, added 8 times the amount of water, extracted the volatile oil by steam distillation, recorded the volume of volatile oil every hour, and observed the oil production. Oil output: brownish-yellow light oil, easy to layered. The oil yield rate of directly extracting oil from sliced pieces was low, with an average oil yield rate of 0.34%; the oil yield rate of 3-5 mm particles was not much different from that of particles below 3 mm, with an average oil yield rate of 0.54%. Therefore, it is appropriate to coarsely chop Cyperi rhizome into particles of less than 5 mm to extract oil. The volatile oil of Cyperi rhizome with different particle sizes no longer increased after 7 hours of extraction, indicating that the extraction was basically complete. 3. Investigation on the extraction of volatile oil from vinegar fried Myrrha: weighing 3 portions of vinegar fried Myrrha, 200 g each, adding 8 times the amount of water, extracting the volatile oil by steam distillation, recording the volume of volatile oil every hour, and observing the oil release phenomenon. Oil output: light green light oil, easy to layer. The average oil yield was 1.35%. The volatile oil no longer increased after 7 hours of extraction, indicating that the extraction was basically complete. In order to illustrate the efficacy of the pharmaceutical composition of the present invention, Beijing University of Traditional Chinese Medicine was entrusted to conduct a functional test using the samples prepared in the examples. Test examples 1. Materials and methods 1.1 General information In order to identify the efficacy of the pharmaceutical composition of the present invention, the granules of Example 1 before tableting and the granules of Example 2 before encapsulation were used as test samples, as well as the granules before tableting prepared by a comparative example of the same medicinal materials beyond the scope of the claims were used as samples and the Health Analysis and Testing Center of Beijing University of Traditional Chinese Medicine was entrusted to conduct efficacy evaluation experiments. The pharmaceutical composition tablets of the present invention are clinically used to treat rheumatoid arthritis. This experiment was conducted by establishing an adjuvant-induced rat joint model (adjuvant arthritis, AA) and a type II collagen-induced rat joint model (collagen induced arthritis, CIA) to study on the efficacy of pharmaceutical composition tablets of the present invention. AA is an ideal arthritis model close to human rheumatoid arthritis. It is mainly mediated by cellular immunity. Its symptoms and pathological manifestations are similar to human rheumatoid arthritis, but its pathogenesis is not consistent. The pathogenesis of animal models of type II collagen-induced arthritis is closer to that of human RA. Therefore, the above two models were selected for research in this experiment. In the AA model, the efficacy evaluation of the preventive administration of the pharmaceutical composition of the present invention was mainly studied. The efficacy of preventive and therapeutic administration was simultaneously evaluated in the CIA model, and a preliminary study was conducted on the efficacy mechanism of the pharmaceutical composition of the present invention during therapeutic administration, providing experimental basis for the clinical treatment of rheumatoid joints. The research results summarize the data based on the "Measures for Approval of New Drugs", "Research Guidelines for New Traditional Chinese Medicines" and "Measures for the Administration of Drug Registration". Experiment 1. Preventive and therapeutic effect of the pharmaceutical composition of the present invention on adjuvant-induced arthritis in rats In Experiment 1, SD rats were used to prepare adjuvants to induce arthritis in rats, and the preventive and therapeutic effects of the pharmaceutical compositions of the present invention in this model were evaluated mainly by observing the volumetric changes in the contralateral toe of the immunized toe and the histological changes in the joints. Experimental material 1. Animals: SD rats, both male and female, weighing 180-200 g, purchased from Beijing Charles River Laboratory Animal Technology Co. with a License No. SCXK(Beijing)2006- 0009. 2. Drugs and reagents: (1) Test drug: The pharmaceutical composition of the present invention is provided by Shijiazhuang Yiling Pharmaceutical Co., Ltd., and the adult dosage is 17 g crude drug / day. The pharmaceutical compositions 1 and 2 of the present invention and the comparative drug group were yellow-brown granules, and each gram was equivalent to 3.5 g of crude drug. The pharmaceutical composition of the present invention was prepared with 0.5% sodium carboxymethylcellulose to the required concentration for use. (2) Positive control drug: Dexamethasone tablets, Tianjin Lisheng Pharmaceutical Co., Ltd., Lot No. 20090105. Specifications: 0.75 mg / tablet. Orally, the starting dose for adults is 0.75 to 3.00 mg (1 to 4 tablets) once, 2 to 4 times a day. The maintenance dose is about 0.75 mg (1 tablet) per day, depending on the condition. (3) Incomplete Freund's adjuvant (IFA) was a sigma product, Lot No. 62K8928. (4) Bacillus calmette-guerin (BCG) vaccine was purchased from China National Institute for the Control of Pharmaceutical and Biological Products (NCICPBP), Lot No. 20110130. (5) PRMI 1640 medium: GIBCO product, Lot 1024455. 100 u / ml penicillin, 100 u / ml streptomycin, 2 mM glutamine were added to the 1640 medium before use, and 10% inactivated fetal bovine serum was added to arrive at the complete 1640 medium. (6) ConA (Lot No. 71K7024) and MTT (Lot No. 66H5033) were from Sigma. (7) Sodium Dodecyl Sulfate (SDS): Serva product, Lot No. 20760. (8) N-N-Dimethylformamide (DMF): Amresco product. 3. Instruments: (1) YLS-7B toe volume measuring instrument was a product of Huaibei Zhenghua Biological Instrument Co., Ltd. (2) CalaxyS type CO2 incubator, RSBiotech company. (3) SCR20BA refrigerated centrifuge, Hitachi, Japan. (4) Biological microscope, Olympus, Japan. (5) DNM type microplate reader, Beijing Perlong New Technology Co., Ltd. (6) Sakura push-pull slicer, Japan. Methods and results (I) Effect of the pharmaceutical composition of the present invention on the toe volume of adjuvant-induced arthritis in rats 1. Preparation of Freund's Complete adjuvant CFA: added BCG vaccine to incomplete Freund's adjuvant (IFA) to make the final concentration 10 mg / ml, and beat repeatedly to form an emulsion. 2. Preparation of rat adjuvant arthritis model (AA): injected 100 µl / animal of the above emulsion subcutaneously into the left sole of each rat to induce adjuvant arthritis in rats. The normal control group received no treatment. 3. Grouping and administration of experimental animals: SD rats were randomly divided into 6 groups. That is, the normal control group was given an equal volume of vehicle; the adjuvant arthritis model group was given an equal volume of vehicle; the pharmaceutical composition 1 of the present invention, the pharmaceutical composition 2 of the present invention, and the comparative drug group, intragastric administration was started the day after the model was prepared, with a dose of 2.26 g / kg, equivalent to 8 times the daily dosage for adults; the positive control group was given Dexamethasone 0.1 mg / kg, equivalent to 8 times the daily dosage for adults. The dosage volume in each group was 1 ml / 100g body weight. 4. The effect of the pharmaceutical composition of the present invention on the toe volume of rats with adjuvant arthritis: before inflammation, the volume of the right hind paw of each rat was measured with a toe volume measuring instrument. After immunization, the volume of the paw was measured every 4 days until the end of 30 days. The changes in foot volume of rats in each group were observed. SPSS10.0 software was used for data analysis. All data results were expressed as mean <com:Math><semantics>±<annotation encoding="application / x-tex">\pm< / annotation>< / semantics>< / com:Math> standard deviation (*<com:Math><semantics>±<annotation encoding="application / x-tex">\pm< / annotation>< / semantics>< / com:Math>*). One-Way ANOVA was used to determine the significance of differences. LSD test was used for pairwise comparisons between groups. P<0.05 was considered a significant difference. The results showed that from 11 days after immunization to the end of the experiment, the contralateral paw of the rats preparing the adjuvant model began to swell gradually. The maximum toe volume occurred 23 days after immunization. After that, as the inflammation subsided, the toe volume gradually decreased. From 15 days after immunization until the end of the experiment, the toe volume of the model group was significantly larger than that of the normal control group (p<0.05 or p<0.01). From 15 days after immunization until the end of the experiment, the toe volume of the Dexamethasone group was significantly smaller than that of the model control group (p<0.01). Group 1 of the pharmaceutical composition of the present invention can significantly reduce the toe volume of rats compared with the model group starting from 15 days after immunization, and continues to 30 days (p<0.05). Group 2 of the pharmaceutical composition of the present invention showed significant decrease compared with the model control group on 15d, 19d, 27d and 30d after immunization (p<0.05). The control drug group had a tendency to inhibit toe swelling, but it was not statistically significant. The results are shown in Tables 1- 1 and 1-2. Table 1-1: Effects of the pharmaceutical composition of the present invention on contralateral foot swelling in rats with adjuvant arthritis (*±*) [Image disponible dans le document PDF, Image available in the PDF document] [Image disponible dans le document PDF, Image available in the PDF document] Note: Model group v.s. the control group, <com:Math><semantics>△p<0.05<annotation encoding="application / x-tex">\triangle p < 0.05< / annotation>< / semantics>< / com:Math>, <com:Math><semantics>△△p<0.01<annotation encoding="application / x-tex">\triangle \triangle p < 0.01< / annotation>< / semantics>< / com:Math>. Groups 1, 2 of pharmaceutical composition of the present invention, Dexamethasone group v.s. model group, *p<0.05, **p<0.01. Table 1-2: Effects of the pharmaceutical composition of the present invention on contralateral foot swelling in rats with adjuvant arthritis [Image disponible dans le document PDF, Image available in the PDF document] Note: model group v.s. the control group, <com:Math><semantics>△p<0.05<annotation encoding="application / x-tex">\triangle p < 0.05< / annotation>< / semantics>< / com:Math>, <com:Math><semantics>△△p<0.01<annotation encoding="application / x-tex">\triangle \triangle p < 0.01< / annotation>< / semantics>< / com:Math>. Groups 1, 2 of pharmaceutical composition of the present invention, Dexamethasone group v.s. model group, *p<0.05, **p<0.01. (II) Effect of the pharmaceutical compositions of the present invention on the proliferation of splenic T-lymphocytes in rats with adjuvant-induced arthritis 1. Preparation of adjuvant arthritis model and grouping and administration of animals: same as Experiment I (1). 2. Effects of the pharmaceutical composition of the present invention on the proliferation of splenic T-lymphocytes in rats with adjuvant arthritis: at the end of the experiment, rats of each group were executed, spleens were taken aseptically, separated into individual cells, erythrocytes were destroyed by the hypotonic method, and the splenic lymphocytes were adjusted to be <com:Math><semantics>5×109<annotation encoding="application / x-tex">5\times10^9< / annotation>< / semantics>< / com:Math> / L, which were added to the 96-well culture plate with 100 µl in each well, and then added the 1640 complete culture medium containing ConA (the final concentration of which was 5 µg / ml), with 100 µl in each well, and incubated for 72 h. 4 h before the end of incubation, 20 µl of 5 mg / ml MTT solution was added to each well, and at the end of incubation, 50 µl of triple dissolution solution (20% SDS-45% DMF, HCl adjusted to pH 2.0) was added to each well, and a colorimetry assay was performed at 570nm after the methazan particles were dissolved at room temperature overnight. SPSS10.0 software was used for data analysis. All data results were expressed as mean <com:Math><semantics>±<annotation encoding="application / x-tex">\pm< / annotation>< / semantics>< / com:Math> standard deviation (*<com:Math><semantics>±<annotation encoding="application / x-tex">\pm< / annotation>< / semantics>< / com:Math>*). One-Way ANOVA was used to determine the significance of differences. LSD test was used for pairwise comparisons between groups. P<0.05 was considered a significant difference. The results showed that the proliferation of spleen T lymphocytes in the adjuvant model group was significantly increased compared with the normal group (p<0.01). Dexamethasone significantly inhibited the proliferation of splenic T lymphocytes in the adjuvant model rats (p<0.01). Groups 1, 2 of the pharmaceutical composition can also significantly inhibit the proliferation of splenic T lymphocytes in adjuvant arthritis model rats (p<0.01 and p<0.05). See Table 2. Table 2: Effect of the pharmaceutical composition of the present invention on lymphocyte proliferation in rats with adjuvant arthritis (*±*) [Image disponible dans le document PDF, Image available in the PDF document] Note: Model group v.s. the control group, <com:Math><semantics>△p<0.05<annotation encoding="application / x-tex">\triangle p < 0.05< / annotation>< / semantics>< / com:Math>, <com:Math><semantics>△△p<0.01<annotation encoding="application / x-tex">\triangle \triangle p < 0.01< / annotation>< / semantics>< / com:Math>. Groups 1, 2 of pharmaceutical composition of the present invention, Dexamethasone group v.s. model group, *p<0.05, **p<0.01. (III) Effects of the pharmaceutical composition of the present invention on the pathological morphology of joint tissue in rats with adjuvant arthritis 1. Preparation of adjuvant arthritis model and grouping and administration of animals: same as Experiment 1 (I). 2. Effects of the pharmaceutical composition of the present invention on the pathological morphology of joint tissue in rats with adjuvant arthritis: the rat AA model was decapitated on the 30th day after modeling, and the right ankle joint was harvested, fixed in formalin, embedded in paraffin, sectioned, and stained with HE. The results showed that the matrix of the joint capsule connective tissue of rats in the normal group was in a colloid state, mainly composed of collagen fibers, with few small blood vessels and a small amount of macrophages, plasma cells, mast cells and lymphocytes. 1-2 layers of synovial cells can be seen in the synovial tissue of the joint. Mature synovial tissue can be seen under the synovium, and a few small blood vessels can be seen. The synovial cells were neatly arranged and flat, the joint surface was smooth, and there was no exudate in the joint cavity. The joint skeletal muscle cells of the rats in the normal group were strip-shaped or block-shaped, with less connective tissue between muscle cells, and fibroblasts and macrophages were occasionally seen in the connective tissue. The connective tissue of the joint capsule of the rats in the model group contained macrophages, plasma cells, and mast cells, and inflammatory cells existed in groups, occupying a large portion of the tissue space. The synovial tissue in the model group was significantly thickened, the synovial cells proliferated significantly, the cell layer increased significantly, the cells swelled, and a large number of lymphocytes, plasma cells, macrophages and a small number of polymorphonuclear leukocytes can be seen infiltrating, fibrous tissue proliferated, small blood vessels increase significantly, synovial layer adhered to cartilage, cartilage degenerated, fibrous oozing can be seen in the articular cavity and synovial invaded cartilage, resulting in the destruction of cartilage and bone, which was mostly manifested as proliferative inflammation. There was less connective tissue between skeletal muscle cells and more between muscle bundles. Fibroblasts and macrophages were occasionally seen in the interfascicular connective tissue, but inflammatory cells often existed in groups, which was exudative inflammation. In the rats in the Dexamethasone group, there were a small number of inflammatory cells scattered in the joint capsule connective tissue matrix; there was less connective tissue between skeletal muscle cells, and no obvious fibroblasts and macrophages were found, which was a normal tissue morphology; there were about 1-3 layers of normal synovial cells in the synovial tissue, which were neatly arranged and regular in cell shape. There was no inflammatory cell infiltration or pannus formation. The Group 1 of pharmaceutical composition of the present invention had basically normal joint capsule connective tissue, rare inflammatory cells, less connective tissue between muscle cells, smooth cartilage tissue surfaces on both sides of the joint, and about 1-3 layers of synovial cells, similar to the normal group. There was a small amount of inflammatory cell infiltration. The Group 2 of pharmaceutical composition of the present invention, there were inflammatory cells scattered in the joint capsule connective tissue and small blood vessels, macrophages, plasma cells, mast cells, etc. were rarely seen. There is less connective tissue between skeletal muscle cells and more between muscle bundles. Fibroblasts and macrophages were occasionally found between connective tissues. There was a small amount of fibrous tissue attached to the surface of articular cartilage tissue, and the intercellular matrix contained a large number of collagen fibers arranged in bundles. In the joint capsule connective tissue of the rats in the control drug group, there were macrophages, plasma cells, and mast cells, and inflammatory cells existed in groups, occupying part of the tissue space. There was less connective tissue between skeletal muscle cells, and fibroblasts and macrophages were occasionally found in the connective tissue. Some areas of the articular cartilage tissue were thin, deeply stained, and had unclear boundaries with the bone cell interstitium. Synovial cells proliferated, and there was fibrous tissue between the cartilages. Summary (1) The contralateral paw of rats with adjuvant arthritis began to swell 11 days after the establishment of the model and continued until the end of the experiment. The maximum toe volume occurred on the 23rd day after immunization. After that, as the inflammation subsided, the toe volume gradually decreased. From 15 days after modeling to the end of the experiment, the toe volume of the model group was significantly larger than that of the normal control group (p<0.05 or p<0.01). The proliferation of spleen T lymphocytes in the adjuvant model group was significantly increased compared with the normal group (p<0.01), indicating that the T cell immunity of the model rats was enhanced. Histology shows that there were a large number of inflammatory cells in the joint capsule connective tissue of rats with adjuvant arthritis, and synovial cells in the joints proliferated significantly, and a large number of lymphocytes, plasma cells, macrophages and a small amount of polymorphonuclear leukocytes can be infiltrated, and fibrotic tissue proliferated and small blood vessels increased significantly. (2) From the 15th day after immunization to the end of the experiment, the toe volume of the positive control drug Dexamethasone group was significantly smaller than that of the model control group (p<0.01); and the proliferation of splenic T lymphocytes of adjuvant model rat could be significantly inhibited. (p<0.01). Histology showed that there were a small number of inflammatory cells scattered in the joint capsule connective tissue, and there were approximately 1-3 layers of synovial cells, neatly arranged, with regular cell morphology, and no obvious inflammatory cell infiltration. (3) The Group 1 of pharmaceutical composition of the present invention can significantly reduce the toe volume of rats compared with the model group starting from 15 days after immunization, and continues to 30 days (p<0.05). The Group 2 of pharmaceutical composition of the present invention significantly decreased compared with the model control group on 15d, 19d, 27d and 30d after immunization (p<0.05). Groups 1, 2 of the pharmaceutical composition of the present invention can also significantly inhibit the proliferation of splenic T lymphocytes in adjuvant arthritis model rats (p<0.01 and p<0.05). Histology showed that the joint capsule connective tissue of pharmaceutical compositions 1 and 2 of the present invention was basically normal, with a small amount of inflammatory cells, and the surface of the articular cartilage tissue was basically normal or slightly damaged, with a small amount of inflammatory cell infiltration and fibrous tissue. Experiment 2. Effect of preventive administration of the pharmaceutical composition of the present invention on type II collagen-induced arthritis in rats In Experiment 2, SD rats were used to prepare a type II collagen-induced rat arthritis model. The preventive and therapeutic effect of the pharmaceutical composition of the present invention on this model was mainly evaluated by observing the immune arthritis index, volume changes of the right toe and joint histological changes. Experimental material 1. Animals: SD rats, both male and female, weighing 180-200 g, purchased from Beijing Charles River Laboratory Animal Technology Co. with a license No. SCXK(Beijing)2006- 0009. 2. Drugs and reagents: (1) Test drug: The pharmaceutical composition of the present invention is provided by Shijiazhuang Yiling Pharmaceutical Co., Ltd., and the adult dosage is 17 g crude drug / day. Group 1 and 2 of the pharmaceutical compositions of the present invention and the comparative drug group were yellow-brown granules, and each gram was equivalent to 3.5 g of crude drug. Lot. No. 110301. The pharmaceutical composition of the present invention was prepared with 0.5% sodium carboxymethylcellulose to the required concentration for use. (2) Positive control drug: Dexamethasone tablets, Tianjin Lisheng Pharmaceutical Co., Ltd., Lot No. 20090105. Specifications: 0.75 mg / tablet. (3) Incomplete Freund's adjuvant (IFA) (Lot No. 62K8928) and acid-soluble type II collagen (collagen II, 3806) (Lot No. 130435) were both sigma products. (4) BCG vaccine was purchased from China National Institute for the Control of Pharmaceutical and Biological Products (NCICPBP), Lot No. 20110130. 3. Instruments: (1) YLS-7B toe volume measuring instrument was a product of Huaibei Zhenghua Biological Instrument Co., Ltd. (2) Sakura push-pull slicer, Japan. Methods and results (I) Effect of the pharmaceutical composition of the present invention on joint index of type II collagen-induced rat arthritis model 1. Preparation of Freund's Complete adjuvant CFA: added BCG vaccine to incomplete Freund's adjuvant (IFA) to make the final concentration 7.5 mg / ml, and beat repeatedly to form an emulsion. 2. Preparation of rat collagen arthritis model: bovine type II collagen was dissolved in 0.1M glacial acetic acid and incubated at 4°C overnight, then it was ground with CFA and made into an emulsion containing 2 mg / ml of type II collagen. 150 µl of the above emulsion was injected subcutaneously into the left foot and the radix of the tail into the immunized rats of the model group and each of the administered groups (each rat was injected with 150 µg of type II collagen), and then 150 µl of the same kind of emulsion was injected into the radix of the tail on the 10th day to strengthen the immunization. The normal control group was left untreated. 3. Grouping and administration of experimental animals: SD rats were randomly divided into 6 groups. That is, the normal control group was given an equal volume of vehicle; the collagen arthritis model group was given an equal volume of vehicle; the pharmaceutical composition 1 of the present invention, the pharmaceutical composition 2 of the present invention, and the comparative drug group were administered intragastrically the next day after the model was prepared, with a dose of 2.26g / kg, equivalent to 8 times the daily dosage for adults; the positive control drug group was administered Dexamethasone 0.1mg / kg, equivalent to 8 times the adult dosage. The dosage volume in each group was 1ml / 100g body weight. 4. Effect of the pharmaceutical composition of the present invention on the arthritis index of rats with collagen arthritis: starting from Day 14 after inflammation, each rat was scored using the joint scoring method. Ears: nodules and redness (No: 0 points, Yes: 1 point); nose: redness and swelling (No: 0 points, Yes: 1 point); tail: nodules (No: 0 points, Yes: 1 point); front paws: inflammation of at least one joint (No: 0 points, Yes: 1 point); right hind paw: swelling (No: 0 points, Mild: 1 point, Moderate: 2 points, Severe: 3 points). The average score for each group of rats was the arthritis index. SPSS10.0 software was used for data analysis. All data results were expressed as mean <com:Math><semantics>±<annotation encoding="application / x-tex">\pm< / annotation>< / semantics>< / com:Math> standard deviation (**±**). One-Way ANOVA was used to determine the significance of differences. LSD test was used for pairwise comparisons between groups. P<0.05 was considered a significant difference. The results showed that about 14 days after the first immunization, type II collagen model rats and rats in each administration group began to develop redness and swelling of the ears and joints, and the redness and swelling of the hind toe joints spread to the forefeet and the tail, and became more serious day by day. In some rats, there were obvious nodules on the tail, which peaked around day 35, followed by a slight reduction in joint swelling until day 50. The arthritis index showed that the type II collagen model group was significantly different from the normal control group from the beginning of 14d to the end of 50d, indicating that the model was successfully prepared. There was no significant difference between the pharmaceutical compositions of the present invention in each administration group from the beginning of immunization to 31d compared with the model group; from 31d to 43d, the arthritis index of the pharmaceutical compositions group 1 of the present invention was significantly reduced compared with that of the model group (p<0.05 and p<0.01); and the pharmaceutical compositions group 2 of the present invention was significantly reduced compared with that of the model group from 35d to 43d (p<0.05). It showed that the pharmaceutical compositions 1 and 2 of the present invention can inhibit the peak of inflammation in rats in the later period caused by type II collagen immunity. However, as the inflammation in the model group gradually subsides, there was no significant difference between the pharmaceutical composition administration group of the present invention and the model group. From the 18th day after immunization until the end of the experiment, the arthritis index of the Dexamethasone group was significantly lower than that of the model group (p<0.01). The results are shown in Tables 3-1 and 3-2. Table 3-1: Effects of preventive administration of the pharmaceutical composition of the present invention on the arthritis index of collagen-induced arthritis in rats (*±*) [Image disponible dans le document PDF, Image available in the PDF document] Note: Model group v.s. the control group, <com:Math><semantics>△p<0.05<annotation encoding="application / x-tex">\triangle p < 0.05< / annotation>< / semantics>< / com:Math>, <com:Math><semantics>△△p<0.01<annotation encoding="application / x-tex">\triangle \triangle p < 0.01< / annotation>< / semantics>< / com:Math>. Groups 1, 2 of pharmaceutical composition of the present invention, Dexamethasone group v.s. model group, *p<0.05, **p<0.01. Table 3-2: Effects of preventive administration of the pharmaceutical composition of the present invention on the arthritis index of collagen-induced arthritis in rats (**±*) [Image disponible dans le document PDF, Image available in the PDF document] Note: Model group v.s. the control group, <com:Math><semantics>△p<0.05<annotation encoding="application / x-tex">\triangle p < 0.05< / annotation>< / semantics>< / com:Math>, <com:Math><semantics>△△p<0.01<annotation encoding="application / x-tex">\triangle \triangle p < 0.01< / annotation>< / semantics>< / com:Math>. Groups 1, 2 of pharmaceutical composition of the present invention, Dexamethasone group v.s. model group, *p<0.05, **p<0.01. (II) Effect of the pharmaceutical composition of the present invention on the toe volume of type II collagen-induced rat arthritis model 1. Preparation of collagen-induced arthritis model in rats and grouping and administration of animals: Same as Experiment 2 (I). 2. The effect of the pharmaceutical composition of the present invention on the toe volume of collagen-induced arthritis rats: before inflammation, the toe volume of the right hind foot of each rat was measured with a toe volume measuring instrument, and the volume of the paw was measured every 4 days from the 11th day after the first immunization to the 50th day. The changes in foot volume of rats in each group were observed. SPSS 10.0 software was used for data analysis. All data results were expressed as mean <com:Math><semantics>±<annotation encoding="application / x-tex">\pm< / annotation>< / semantics>< / com:Math> standard deviation (*<com:Math><semantics>±<annotation encoding="application / x-tex">\pm< / annotation>< / semantics>< / com:Math>*). One- Way ANOVA was used to determine the significance of differences. LSD test was used for pairwise comparisons between groups. P<0.05 was considered a significant difference. The results showed that there was no significant difference in toe volume between groups from Day 11 to Day 14 after the first immunization (data not shown). From Day 18 after the first immunization to the end of the experiment, the toe volume of the collagen arthritis model group rats was significantly higher than that of the control group rats, indicating that the model rats had an inflammatory reaction in the toes, and the maximum toe volume occurred Day 35 to Day 39 after immunization. After that, as the inflammation subsided, the toe volume gradually decreased. From Day 18 after the first immunization to the end of the experiment, the toe volume of the Dexamethasone group was significantly smaller than that of the collagen arthritis model group (p<0.01). Due to long-term use of Dexamethasone, the rats in this group lost weight, so that the toe volume was even smaller than that of the normal control group. The Group 1 of pharmaceutical composition of the present invention can significantly reduce the toe volume of rats compared with the model group starting from Day 22 after immunization, and continues to Day 43 (p<0.05). The Group 2 of pharmaceutical composition of the present invention can significantly reduce the toe volume of rats compared with the model group starting from Day 26 after immunization, and continues to Day 39 (p<0.05). However, as the inflammation in the model group subsided, there was no significant difference in the inhibitory effect of the pharmaceutical compositions 1 and 2 of the present invention on toe swelling compared with the model group. The effect of the comparative drug group on inhibiting toe swelling was not obvious. The results are shown in Tables 4-1 and 4-2. Table 4-1: Effects of preventive administration of the pharmaceutical composition of the present invention on the volume of the toes of the right foot of collagen-induced arthritis in rats <com:Math><semantics>(ẋ±s)<annotation encoding="application / x-tex">(\dot{x} \pm s)< / annotation>< / semantics>< / com:Math> [Image disponible dans le document PDF, Image available in the PDF document] [Image disponible dans le document PDF, Image available in the PDF document] Note: Model group v.s. the control group, <com:Math><semantics>△p<0.01<annotation encoding="application / x-tex">\triangle p < 0.01< / annotation>< / semantics>< / com:Math>. Groups 1, 2 of pharmaceutical composition of the present invention, Dexamethasone group v.s. model group, *p<0.05, **p<0.01. Table 4-2: Effects of preventive administration of the pharmaceutical composition of the present invention on the volume of the toes of the right foot of collagen-induced arthritis in rats <com:Math><semantics>(x±s)<annotation encoding="application / x-tex">(x \pm s)< / annotation>< / semantics>< / com:Math> [Image disponible dans le document PDF, Image available in the PDF document] Note: Model group v.s. the control group, <com:Math><semantics>△p<0.01<annotation encoding="application / x-tex">\triangle p < 0.01< / annotation>< / semantics>< / com:Math>. Groups 1, 2 of pharmaceutical composition of the present invention, Dexamethasone group v.s. model group, *p<0.05, **p<0.01. (III) Effect of the pharmaceutical composition of the present invention on joint tissue pathology of type II collagen-induced rat arthritis model 1. Preparation of collagen-induced arthritis model in rats and grouping and administration of animals: Same as Experiment 2 (I). 2. Effects of the pharmaceutical composition of the present invention on the pathological morphology of joint tissue in rats with collagen-induced arthritis: the rat models in each experimental group were decapitated on the 50th day after modeling, and the right ankle joints were harvested, fixed in formalin, embedded in paraffin, sectioned, and stained with HE. The results showed that the connective tissue of the normal group contains a small number of macrophages, plasma cells, mast cells and lymphocytes, and there was less connective tissue between muscle cells, 1-2 layers of synovial cells can be seen in the articular cartilage, the joint surface was smooth, and there was no exudate in the joint cavity. In the collagen model group, inflammatory cell infiltration can be seen in the joint connective tissue and muscle tissue, and in the articular cartilage, neutrophils and monocytes, especially lymphocytes, can be seen infiltrating in the synovial tissue, blood vessels increased, vascular intima deformed and proliferated, and the lumen became narrowed or blocked, accompanied by the formation of pannus, a large amount of cellulose leaked out and collagen fibers were deposited under the synovial cells. In the Dexamethasone group, the joint connective tissue and muscle tissue were basically normal, there was slight proliferation of synovial cells in the articular cartilage, and the infiltration of inflammatory cells was not obvious. In Groups 1, 2 of the pharmaceutical composition of the present invention, there was a small amount of inflammatory cell infiltration in the joint connective tissue, the muscle tissue was basically normal, there was mild proliferation of synovial cells, inflammatory cell infiltration and a small amount of fibroplasia, and mild blood vessel proliferation in the joint cavity. In the comparative drug group, there were more inflammatory cell infiltrations in joint connective tissue and muscle tissue, and joint synovial cell proliferation was accompanied by inflammatory cell infiltration. Groups 1, 2 of the pharmaceutical composition of the present invention had a better effect on improving tissue damage in collagen arthritis. Summary (1) The arthritis index of the collagen-induced arthritis model rats started to be significantly higher than that of the normal control group on about Day 14 after the first immunization, and the toe volume started to be significantly higher than that of the normal control group on Day 18 after the first immunization. The significant difference was maintained until the end of the experiment (<com:Math><semantics>p<0.01<annotation encoding="application / x-tex">p<0.01< / annotation>< / semantics>< / com:Math>). The arthritis index and toe volume of the model group reached a peak around Day 35 to Day 39 after the first immunization. After that, as the inflammation subsided, the arthritis index and toe volume decreased. Pathological observation showed: inflammatory cell infiltration in the connective tissue and muscle tissue of the model rats, joint synovial tissue hyperplasia and inflammatory cell infiltration, increased blood vessels accompanied by pannus formation, massive exudation of cellulose under the synovial cells, and deposition of collagen fibers. This indicates that the modeling was successful. (2) The positive control drug Dexamethasone can significantly inhibit arthritis index and reduce toe volume starting from Day 18 of the first immunization, and its inhibitory effect was maintained until the end of the experiment. There were significant differences compared with the model group (p<0.01). Pathological observation showed that in the Dexamethasone group, the joint connective tissue and muscle tissue were basically normal, there was slight proliferation of synovial cells in the articular cartilage, and the infiltration of inflammatory cells was not obvious. (3) The Group 1 of pharmaceutical composition of the present invention significantly reduced the arthritis index of arthritic rats from Day 31 to Day 43 after the first immunization, and the Group 2 of pharmaceutical composition of the present invention significantly reduced the arthritis index of arthritic rats from Day 35 to Day 43 after the first immunization (p <com:Math><semantics><0.05<annotation encoding="application / x-tex">< 0.05< / annotation>< / semantics>< / com:Math> and p<0.01). The Group 1 of pharmaceutical composition of the present invention can significantly reduce the toe volume of rats compared with the model group starting from Day 22 after the first immunization, and this continues until Day 43 (p<0.05), and the Group 2 of pharmaceutical composition of the present invention can significantly reduce the toe volume of rats compared with the model group starting from Day 26 after the first immunization and continuing to Day 39 (p<0.05). Thereafter, as the inflammation in the model gradually decreased, there was no significant difference between the control drug group and the model group. The pathological results showed that there was a small amount of inflammatory cell infiltration in the joint connective tissue of Groups 1, 2 of the pharmaceutical composition of the present invention, and the muscle tissue was basically normal, and there was mild proliferation of synovial cells, inflammatory cell infiltration and a small amount of fibroplasia, and mild blood vessel proliferation in the joint cavity. Experiment 3. Effect and mechanism of therapeutic administration of the pharmaceutical composition of the present invention on type II collagen-induced arthritis in rats In Experiment 3, pure line Lewis rats were used to prepare a type II collagen-induced rat arthritis model. The therapeutic effect of the pharmaceutical composition of the present invention on this model was evaluated by observing the arthritis index and the volume change of the right toe, and preliminary research on its therapeutic mechanism was conducted through observation. Experimental material 1. Animals: Lewis rats, male, weighing 180-200 g, purchased from Beijing Charles River Laboratory Animal Technology Co. Animal certificate number: License No. SCXK(Beijing)2006-0009. 2. Drugs and reagents: (1) Test drug: The pharmaceutical composition of the present invention is provided by Shijiazhuang Yiling Pharmaceutical Co., Ltd., and the adult dosage is 17 g crude drug / day. The pharmaceutical compositions 1 and 2 of the present invention and the comparative drug group were yellow-brown granules, and each gram was equivalent to 3.5 g of crude drug. Lot. No. 110301. The pharmaceutical composition of the present invention was prepared with 0.5% sodium carboxymethylcellulose to the required concentration for use. (2) Positive control drug: Dexamethasone tablets, Tianjin Lisheng Pharmaceutical Co., Ltd., Lot No. 20090105. Specifications: 0.75 mg / tablet. (3) Incomplete Freund's adjuvant (IFA) was a sigma product, Lot No. 62K8928. (4) Acid-soluble type II collagen (collagen II, 3806) (Lot No. 130435) and MTT (66H5033) were Sigma products. (5) BCG vaccine was purchased from China National Institute for the Control of Pharmaceutical and Biological Products (NCICPBP), Lot No. 20110130. (6) PRMI1640 medium: GIBCO product, Lot No. 1024455. Before use, 100u / ml penicillin, 100u / ml streptomycin, and 2mM glutamine were added to the 1640 culture medium. 10% inactivated fetal bovine serum was added to the complete 1640 culture medium. (7) Sodium dodecyl sulfate (SDS): Serva product, Lot No. 20760. (8) N-N-dimethylformamide (DMF): Amresco product. (9) Rat IL-1 cytokine ELISA kit (Lot No. 1209145), TNF-α cytokine ELISA kit (Lot No. 1210132) and IL-10 cytokine ELISA kit (Lot No. 1210162) were purchased from Beijing Bangding Taike Biotechnology Technology Co., Ltd. (10) Horseradish enzyme (HRP)-labeled goat anti-rat IgG antibody (Lot No. 20111002) and goat anti-rat IgM (Lot No. 20111015) were purchased from Beijing Boya Xiangda Biotechnology Co., Ltd. 3. Instruments: (1) YLS-7B toe volume measuring instrument was a product of Huaibei Zhenghua Biological Instrument Co., Ltd. (2) CalaxyS type CO2 incubator, RSBiotech company. (3) SCR20BA refrigerated centrifuge, Hitachi, Japan. (4) Biological microscope, Olympus, Japan. (5) DNM type microplate reader, Beijing Perlong New Technology Co., Ltd. Methods and results (I) Effect of the administration of the pharmaceutical composition of the present invention on joint index of collagen-induced rat arthritis model 1. Preparation of rat type II collagen-induced arthritis model: Same as Experiment 2 (I). 2. Grouping and administration of experimental animals: Lewis rats were randomly divided into 6 groups. That is, the normal control group was given an equal volume of vehicle; the collagen-induced arthritis model group was given an equal volume of vehicle; on Day 14 after the model was prepared, the pharmaceutical compositions 1 and 2 of the present invention and the control drug group were administered by gavage at a dose of 2.26g / kg, equivalent to 8 times the daily dosage for adults; the positive control drug Dexamethasone group was given Dexamethasone 0.1 mg / kg, equivalent to 8 times the daily dosage for adults. The dosage volume in each group was 1 ml / 100g body weight. 3. Effect of the pharmaceutical composition of the present invention on the arthritis index of rats with collagen arthritis: starting from Day 14 after inflammation, each rat was scored using the joint scoring method. Ears: nodules and redness (No: 0 points, Yes: 1 point); nose: redness and swelling (No: 0 points, Yes: 1 point); tail: nodules (No: 0 points, Yes: 1 point); front paws: inflammation of at least one joint (No: 0 points, Yes: 1 point); right hind paw: swelling (No: 0 points, Mild: 1 point, Moderate: 2 points, Severe: 3 points). The average score for each group of rats was the arthritis index. SPSS10.0 software was used for data analysis. All data results were expressed as mean <com:Math><semantics>±<annotation encoding="application / x-tex">\pm< / annotation>< / semantics>< / com:Math> standard deviation (*<com:Math><semantics>±<annotation encoding="application / x-tex">\pm< / annotation>< / semantics>< / com:Math>*). One-Way ANOVA was used to determine the significance of differences. LSD test was used for pairwise comparisons between groups. P<0.05 was considered a significant difference. The results showed that type II collagen-induced arthritis model rats began to develop arthritis symptoms about 14 days after the first immunization, reaching a peak around Day 35, and then joint swelling was slightly reduced and continued until Day 50. The arthritis index showed that the model group had significant differences from the normal control group from Day 14 to the end of Day 50 of the experiment, indicating that the model was successfully prepared. From Day 22 after Dexamethasone autoimmunization until the end of the experiment, the arthritis index was significantly lower than that of the model group (p<0.05 or p<0.01). The arthritis index of the Group 1 of pharmaceutical composition of the present invention was significantly reduced (p<0.05 and p<0.01) compared with the model group from Day 35 (21 days after administration) until Day 47. The Group 2 of pharmaceutical composition of the present invention had significantly reduced symptoms from Day 39 (25 days after administration) to Day 43 compared with the model group (p<com:Math><semantics><0.05<annotation encoding="application / x-tex"><0.05< / annotation>< / semantics>< / com:Math>). There was also a decreasing trend in the control drug group, but there was no significant difference. It showed that the pharmaceutical compositions 1 and 2 of the present invention can inhibit the peak of inflammation in rats caused by type II collagen immunity in the later period. However, as the inflammation in the model gradually subsided, there was no difference between the pharmaceutical compositions 1 and 2 of the present invention and the model group. The results were shown in Tables 5-1 and 5-2. Table 5-1: Effects of therapeutic administration of the pharmaceutical composition of the present invention on arthritis index in type II collagen-induced arthritis model rats (**±*) [Image disponible dans le document PDF, Image available in the PDF document] Note: Model group v.s. the control group, <com:Math><semantics>△p<0.01<annotation encoding="application / x-tex">\triangle p < 0.01< / annotation>< / semantics>< / com:Math>. Groups 1, 2 of pharmaceutical composition of the present invention, Dexamethasone group v.s. model group, *p<0.05, **p<0.01. Table 5-2: Effects of therapeutic administration of the pharmaceutical composition of the present invention on arthritis index in type II collagen-induced arthritis model rats (**±*) [Image disponible dans le document PDF, Image available in the PDF document] Note: Model group v.s. the control group, <com:Math><semantics>△p<0.01<annotation encoding="application / x-tex">\triangle p < 0.01< / annotation>< / semantics>< / com:Math>. Groups 1, 2 of pharmaceutical composition of the present invention, Dexamethasone group v.s. model group, *p<0.05, **p<0.01. (II) Effect of the pharmaceutical composition of the present invention on the toe volume of type II collagen-induced rat arthritis model 1. Preparation of collagen-induced arthritis model in rats and grouping and administration of animals: Same as Experiment 3 (I). 2. The effect of the pharmaceutical composition of the present invention on the toe volume of collagen-induced arthritis rats: before inflammation, the toe volume of the right hind foot of each rat was measured with a toe volume measuring instrument, and the volume of the paw was measured every 4 days from Day 11 after the first immunization to Day 50. The changes in foot volume of rats in each group were observed. SPSS10.0 software was used for data analysis. All data results were expressed as mean <com:Math><semantics>±<annotation encoding="application / x-tex">\pm< / annotation>< / semantics>< / com:Math> standard deviation (*<com:Math><semantics>±<annotation encoding="application / x-tex">\pm< / annotation>< / semantics>< / com:Math>*). One-Way ANOVA was used to determine the significance of differences. LSD test was used for pairwise comparisons between groups. P<0.05 was considered a significant difference. The results showed that there was no significant difference in toe volume between groups from Day 11 to Day 14 after the first immunization (data not shown). From Day 18 after the first immunization to the end of the experiment, the toe volume of the collagen arthritis model group rats was significantly higher than that of the control group rats, indicating that the model rats had an inflammatory reaction in the toes, and the maximum toe volume occurred Day 35 to Day 39 after immunization. After that, as the inflammation subsided, the toe volume gradually decreased. From Day 22 after Dexamethasone immunization (8 days after administration) until the end of the experiment, the toe volume was significantly smaller than that of the arthritis model group (p<com:Math><semantics><0.05<annotation encoding="application / x-tex"><0.05< / annotation>< / semantics>< / com:Math> or p<com:Math><semantics><0.01<annotation encoding="application / x-tex"><0.01< / annotation>< / semantics>< / com:Math>). The Group 1 of pharmaceutical composition of the present invention can significantly reduce the toe volume of rats compared with the model group starting from Day 35 after immunization (21 days after administration), and continues to Day 47 (p<0.05). The Group 2 of pharmaceutical composition of the present invention can significantly reduce the toe volume of rats compared with the model group starting from Day 39 after immunization (25 days after administration), and continues to Day 50 (p<com:Math><semantics><<annotation encoding="application / x-tex"><< / annotation>< / semantics>< / com:Math>0.05). The effect of the control drug group on inhibiting toe swelling was not obvious. The results are shown in Tables 6-1 and 6-2. Table 6-1: Effects of therapeutic administration of the pharmaceutical composition of the present invention on the volume of the toes of the right foot of collagen-induced arthritis in rats (1115) [Image disponible dans le document PDF, Image available in the PDF document] [Image disponible dans le document PDF, Image available in the PDF document] Note: Model group v.s. the control group, <com:Math><semantics>△p<0.01<annotation encoding="application / x-tex">\triangle p < 0.01< / annotation>< / semantics>< / com:Math>. Groups 1, 2 of pharmaceutical composition of the present invention, Dexamethasone group v.s. model group, *p<0.05, **p<0.01. Table 6-2: Effects of the rapeutic administration of the pharmaceutical composition of the present invention on the volume of the toes of the right foot of collagen-induced arthritis in rats <com:Math><semantics>(x±s)<annotation encoding="application / x-tex">(x \pm s)< / annotation>< / semantics>< / com:Math> [Image disponible dans le document PDF, Image available in the PDF document] Note: Model group v.s. the control group, <com:Math><semantics>△p<0.01<annotation encoding="application / x-tex">\triangle p < 0.01< / annotation>< / semantics>< / com:Math>. Groups 1, 2 of pharmaceutical composition of the present invention, Dexamethasone group v.s. model group, *p<0.05, **p<0.01. (III) Effect of the pharmaceutical composition of the present invention on the proliferation of type II collagen-specific splenic lymphocytes in the collagen-induced arthritis model 1. Preparation of collagen-induced arthritis model and grouping and administration of animals: Same as Experiment 3 (I). 2. Effect of the pharmaceutical composition of the present invention on the proliferation of splenic lymphocytes in collagen-induced rat arthritis model: Reference literature at the end of the experiment, rats in each group were sacrificed, the spleens were taken aseptically, separated into single cells, and the red blood cells were destroyed by hypotonic method. Spleen lymphocytes were adjusted to <com:Math><semantics>5×109<annotation encoding="application / x-tex">5\times10^9< / annotation>< / semantics>< / com:Math> / L, added to a 96-well culture plate with 100µl each well, and complete culture medium containing type II collagen was added at 100µl / well to make the final concentration of type II collagen 2.5µg / ml, and then cultured for 72 hours. 4 hours before the end of the culture, 20µl of 5mg / ml MTT solution were added to each well. After the culture, 50µl of triple dissolving solution (20% SDS-45% DMF, HCl to adjust pH to 2.0) were added to each well, and it was left at room temperature overnight, after the formazan particles were dissolved, the color was measured at a wavelength of 570nm. SPSS10.0 software was used for data analysis. All data results were expressed as mean <com:Math><semantics>±<annotation encoding="application / x-tex">\pm< / annotation>< / semantics>< / com:Math> standard deviation ( *<com:Math><semantics>±<annotation encoding="application / x-tex">\pm< / annotation>< / semantics>< / com:Math>s). One-Way ANOVA was used to determine the significance of differences. LSD test was used for pairwise comparisons between groups. P<0.05 was considered a significant difference. The results showed that the proliferation capacity of lymphocytes stimulated by type II collagen in the rat spleen was significantly higher than that in the normal group (p<0.01), indicating that type II collagen-specific lymphocytes were activated in the model mice and that there was a type II collagen-specific cellular immune response in the model mice. Dexamethasone significantly inhibited the proliferative response of splenic lymphocytes induced by type II collagen (p<0.01). Groups 1, 2 of the pharmaceutical composition of the present invention significantly inhibited the proliferation response of type II collagen-specific lymphocytes in the spleen of collagen model rats (<com:Math><semantics>p<0.05<annotation encoding="application / x-tex">p<0.05< / annotation>< / semantics>< / com:Math> or <com:Math><semantics>p<0.01<annotation encoding="application / x-tex">p<0.01< / annotation>< / semantics>< / com:Math>). Table 7: Effect of the pharmaceutical composition of the present invention on the proliferation of spleen lymphocytes in rats with collagen arthritis (*±*) [Image disponible dans le document PDF, Image available in the PDF document] Note: Model group v.s. the control group, <com:Math><semantics>△p<0.01<annotation encoding="application / x-tex">\triangle p < 0.01< / annotation>< / semantics>< / com:Math>. Comparison of pharmaceutical composition groups of the present invention, Dexamethasone group and model group, *p<0.05, **p<0.01. (IV) Effect of the pharmaceutical composition of the present invention on serum anti-type II collagen antibodies in collagen-induced arthritis model rats 1. Preparation of collagen-induced arthritis model and grouping and administration of animals: Same as Experiment 3 (I). 2. Effect of the pharmaceutical composition of the present invention on type II collagen antibodies in the serum of collagen-induced rat arthritis model: At the end of the experiment, blood was collected from the abdominal aorta of the rats after anesthesia, the serum was separated, and the anti-type II collagen antibodies in serum were measured by ELISA. The serum was heat-inactivated and then the antibody content was detected by ELISA. Microplate 96-well plates were coated with 2.5 µg / ml type II collagen at 4°C overnight, blocked with 1% BSA, and the serum was diluted 1:100 in PBS and added to the wells, and incubated at 37°C for 2 hours. 1:8000 diluted horseradish enzyme (HRP)-labeled goat anti-rat IgG antibody was added, and incubate at 37°C for 1 hour; OPD reaction substrate was added and the reaction was terminated with 2N sulfuric acid after 30 minutes; the optical density (OD) value at 492nm was read with a microplate reader. SPSS10.0 software was used for data analysis. All data results were expressed as mean <com:Math><semantics>±<annotation encoding="application / x-tex">\pm< / annotation>< / semantics>< / com:Math> standard deviation (*<com:Math><semantics>±<annotation encoding="application / x-tex">\pm< / annotation>< / semantics>< / com:Math>*). One-Way ANOVA was used to determine the significance of differences. LSD test was used for pairwise comparisons between groups. P<0.05 was considered a significant difference. The results showed that the type II collagen antibody content in the serum of rats in the collagen model group was significantly higher than that in the normal group (<com:Math><semantics>p<0.01<annotation encoding="application / x-tex">p<0.01< / annotation>< / semantics>< / com:Math>). Dexamethasone significantly inhibited the production of type II collagen antibodies in collagen model rats (p<0.01). Groups 1, 2 of the pharmaceutical composition of the present invention and the control drug group can significantly inhibit the production of type II collagen antibodies in the serum of collagen- induced arthritis rat model (p<0.05 or p<0.01). See Table 8. Table 8: Effect of the pharmaceutical composition of the present invention on type II collagen antibodies in the serum of collagen arthritis rats (*±*) [Image disponible dans le document PDF, Image available in the PDF document] Note: Model group v.s. the control group, <com:Math><semantics>△p<0.01<annotation encoding="application / x-tex">\triangle p < 0.01< / annotation>< / semantics>< / com:Math>. Groups 1, 2 of pharmaceutical composition of the present invention, Dexamethasone group v.s. model group, *p<0.05, **p<0.01. (V) Effects of the pharmaceutical composition of the present invention on cytokines in the serum of collagen-induced arthritis model rats Tumor necrosis factor-<com:Math><semantics>α<annotation encoding="application / x-tex">\alpha< / annotation>< / semantics>< / com:Math> (TNF-<com:Math><semantics>α<annotation encoding="application / x-tex">\alpha< / annotation>< / semantics>< / com:Math>) and interleukin-1 (IL-1) play important roles in the pathogenesis and joint damage of rheumatoid arthritis. TNF-<com:Math><semantics>α<annotation encoding="application / x-tex">\alpha< / annotation>< / semantics>< / com:Math> and IL-1 can participate in the pathogenesis and progression of rheumatoid arthritis by activating endothelial cells and promoting the synthesis and release of inflammatory factors. IL-10 is an important inhibitory cytokine that can downregulate the immune response and improve the inflammatory response of arthritis. 1. Preparation of collagen-induced arthritis model and grouping and administration of animals: Same as Experiment 3 (I). 2. Effect of the pharmaceutical composition of the present invention on cytokines in the serum of collagen-induced arthritis rats: at the end of the experiment, blood was collected from the abdominal aorta of the rats after anesthesia, and the serum was separated. The contents of cytokines IL-1, TNF-<com:Math><semantics>α<annotation encoding="application / x-tex">\alpha< / annotation>< / semantics>< / com:Math>, and IL-10 in the serum were measured according to the instructions of the ELISA kit. SPSS10.0 software was used for data analysis. All data results were expressed as mean <com:Math><semantics>±<annotation encoding="application / x-tex">\pm< / annotation>< / semantics>< / com:Math> standard deviation (*<com:Math><semantics>±<annotation encoding="application / x-tex">\pm< / annotation>< / semantics>< / com:Math>*). One-Way ANOVA was used to determine the significance of differences. LSD test was used for pairwise comparisons between groups. P<0.05 was considered a significant difference. The results showed that the serum levels of inflammatory cytokines IL-1 and TNF-<com:Math><semantics>α<annotation encoding="application / x-tex">\alpha< / annotation>< / semantics>< / com:Math> in the model group were significantly higher than those in the normal control group (p<0.01), while Dexamethasone significantly reduced the serum levels of IL-1 and TNF-<com:Math><semantics>α<annotation encoding="application / x-tex">\alpha< / annotation>< / semantics>< / com:Math> (p <0.01), Groups 1, 2 of the pharmaceutical composition of the present invention can also significantly reduce the levels of IL-1 and TNF-<com:Math><semantics>α<annotation encoding="application / x-tex">\alpha< / annotation>< / semantics>< / com:Math> in serum (p<0.05). The inhibitory cytokine IL-10 in the serum of the model group was significantly lower than that of the control group (p<0.01), but each group of the pharmaceutical composition of the present invention and Dexamethasone had no significant improvement effect on the reduction of IL-10 in the serum of model rats (<com:Math><semantics>p>0.05<annotation encoding="application / x-tex">p>0.05< / annotation>< / semantics>< / com:Math>). See Table 9. Table 9: Effect of the pharmaceutical composition of the present invention on serum cytokines in collagen arthritis model rats (*±*) [Image disponible dans le document PDF, Image available in the PDF document] [Image disponible dans le document PDF, Image available in the PDF document] Note: Model group v.s. the control group, <com:Math><semantics>△p<0.01<annotation encoding="application / x-tex">\triangle p < 0.01< / annotation>< / semantics>< / com:Math>. Groups 1, 2 of pharmaceutical composition of the present invention, Dexamethasone group v.s. model group, *p<0.05, **p<0.01. (VI) Effects of the pharmaceutical composition of the present invention on IgG and IgM rheumatoid factors in the serum of collagen-induced rat arthritis model Rheumatoid factor (RF) produced in patients with rheumatoid arthritis is the most common type of autoantibodies and is an autoantibody directed against the Fc segment of IgG. RF can form immune complexes, activate complement, and lead to the development of vasculitis. There are two main types of RF: IgG and IgM. IgM rheumatoid factor appears first in the course of rheumatoid disease, followed by IgG rheumatoid factor later in the disease. The contents of these two types of rheumatoid factors are closely related to the pathogenesis of rheumatoid arthritis. 1. Preparation of collagen-induced arthritis model and grouping and administration of animals: Same as Experiment 3 (I). 2. Effects of the pharmaceutical composition of the present invention on IgG and IgM rheumatoid factors in the serum of rats with collagen-induced arthritis: at the end of the experiment, blood was collected from the abdominal aorta of the rats after anesthesia, and the serum was separated. The purified rabbit IgG was dissolved in PBS solution, thermally denatured at 63°C for 20 minutes, precipitated by adding 0.36 mol / L Na<com:Sub>2< / com:Sub>SO<com:Sub>4< / com:Sub> salt solution, and centrifuged at 10000r / min for 20 minutes, the supernatant was discard, the precipitate was dissolved in the coating solution (20 µg / ml), and the polystyrene plate was coated overnight at 4°C, then blocked with 1% BSA, the rat serum to be tested was diluted with PBS 1:100, added to the drop well, and incubate at 37°C for 2 hours. Then 1:8000 diluted horseradish enzyme (HRP)-labeled goat anti-rat IgG antibody or goat anti-rat IgM was added, and incubated at 37°C for 1 hour; OPD reaction substrate was added, and the reaction was terminated with 2N sulfuric acid after 30 minutes; the optical density (OD) value was read at 492 nm using a microplate reader. SPSS10.0 software was used for data analysis. All data results were expressed as mean <com:Math><semantics>±<annotation encoding="application / x-tex">\pm< / annotation>< / semantics>< / com:Math> standard deviation ( <com:Math><semantics>±±s<annotation encoding="application / x-tex">\pm \pm s< / annotation>< / semantics>< / com:Math> ). One-Way ANOVA was used to determine the significance of differences. LSD test was used for pairwise comparisons between groups. P<0.05 was considered a significant difference. The results showed that IgG and IgM rheumatoid factors were significantly increased in the serum of rats with collagen-induced arthritis, and Dexamethasone could significantly inhibit the production of IgG and IgM rheumatoid factors (p<0.01). The pharmaceutical combination groups 1 and 2 of the present invention can also significantly inhibit the production of IgG and IgM rheumatoid factor in the serum of collagen-induced arthritis model rats (p<0.05 or p<0.01). Table 10: Effect of the pharmaceutical composition of the present invention on serum IgG and IgM rheumatoid factor in rats with collagen arthritis (*±*) [Image disponible dans le document PDF, Image available in the PDF document] Note: Model group v.s. the control group, <com:Math><semantics>△p<0.01<annotation encoding="application / x-tex">\triangle p < 0.01< / annotation>< / semantics>< / com:Math>. Comparison of pharmaceutical composition groups of the present invention, Dexamethasone group and model group, *p<0.05, **p<0.01. Summary (1) A type II collagen-induced rat arthritis model was established using Lewis rats and found that the model rats began to develop arthritis symptoms approximately 14 days after the first immunization and continued until Day 50. The arthritis index and toe volume were significantly higher than those of the control rats. The proliferation of type II collagen-specific splenic lymphocytes in model rats was significantly higher than that of the control group; type II collagen-specific antibodies, IgG and IgM rheumatoid factors, inflammatory factors IL-1 and TNF-<com:Math><semantics>α<annotation encoding="application / x-tex">\alpha< / annotation>< / semantics>< / com:Math> in serum were all significantly higher than those in the control group (p<0.01), and regulatory cytokine IL-10 in serum was significantly lower than that in the control group. The above results show that the type II collagen-induced rat joint model was successfully established, and the model rats had significant inflammatory responses and specific immune responses and inflammatory responses against type II collagen. (2) The arthritis index of the positive control drug Dexamethasone was significantly lower than that of the model group from 22 days after autoimmunization until the end of the experiment (p<0.05 or p<0.01). From 22 days after immunization (8 days after administration) to the end of the experiment, the toe volume was significantly smaller than that of the arthritis model group (p<0.05 or p<0.01). Dexamethasone also significantly inhibited the splenic lymphocyte proliferation response induced by type II collagen (p<0.01), the production of type II collagen antibodies in the serum (<com:Math><semantics>p<0.01<annotation encoding="application / x-tex">p<0.01< / annotation>< / semantics>< / com:Math>), the production of inflammatory cytokines IL-1 and TNF-α (p<0.01) and rheumatoid factors IgG and IgM (p<0.01) in serum, but had no significant effect on the regulatory cytokine IL-10. (3) The arthritis index of the Group 1 of pharmaceutical composition of the present invention was significantly reduced compared with the model group from Day 35 (21 days of administration) to Day 47, and that of the Group 2 of pharmaceutical composition of the present invention from Day 39 (25 days of administration) to Day 43 (p<0.05 and p<0.01). The Group 1 of pharmaceutical composition of the present invention started from Day 35 after immunization (21 days after administration) to Day 47. The Group 2 of pharmaceutical composition of the present invention significantly reduced the toes volume of rats compared with the model group from Day 39 (25 days after administration) to Day 50 after immunization (p<0.05). Groups 1, 2 of the pharmaceutical composition of the present invention significantly inhibited the proliferation response of type II collagen-specific lymphocytes in the spleen of collagen model rats (p<0.05 or p<0.01), the production of type II collagen antibodies in serum (p<0.05 or p<0.01), and the levels of inflammatory cytokines IL-1 and TNF-<com:Math><semantics>α<annotation encoding="application / x-tex">\alpha< / annotation>< / semantics>< / com:Math> in serum (p<0.05), and the production of rheumatoid factor IgG and IgM (p<0.05 or p<0.01). However, it had no obvious improvement effect on the reduction of regulatory cytokine IL-10 in the serum of model rats. Conclusion Rheumatoid arthritis (RA) is a multisystem inflammatory autoimmune disease that mainly affects surrounding joints. The main characteristics of RA are joint inflammatory response and synovial angiogenesis, which in turn lead to chronic synovial hyperplasia, further affecting cartilage and bone, leading to joint deformity and loss of function as the basic pathological changes of the disease. Rat adjuvant arthritis (AA) is an ideal arthritis model close to human rheumatoid arthritis. It can basically reflect the pathological changes of human rheumatoid arthritis. The main mechanism of adjuvant arthritis is the activation of T cells by Mycobacterium tuberculosis. Activated T cells participate in the pathogenesis of RA by releasing cytokines and activating macrophages. AA is therefore primarily mediated by cellular immunity. This model is easy to operate and cheap. The AA model has a rapid onset after inflammation, that is, secondary inflammatory reactions in the contralateral paws gradually appear 10 days after the antigen challenge. The peak of inflammation generally occurs at 20 to 25 days, and then the inflammatory reaction in the rat paws gradually subsides. Although the symptoms and pathological manifestations of AA models are similar to those of human rheumatoid arthritis, their pathogenesis is not consistent. Type II collagen-induced arthritis (CIA) animal model is currently recognized as an ideal animal model for studying the pathogenesis of RA and developing new drugs to treat RA. This model is induced by type II collagen (Collagen II, CII), which is the main component of cartilage and an autoantigen in the pathogenesis of rheumatoid arthritis. Type II collagen antibodies can be detected in the serum and synovial fluid of patients with clinical rheumatoid arthritis. Because the pathogenesis of the CIA model is closer to that of human RA, it has become the preferred model for studying rheumatoid arthritis in recent years. CIA arthritis develops more slowly in rats than in the AA model, with swollen joints starting to occur approximately 2-3 weeks after the first immunization. Its pathological manifestations include progressive synovitis and synovial hyperplasia, inflammatory cell infiltration, cartilage destruction, and ultimately joint damage and stiffness. After the establishment of CIA, joint inflammation in rats will remain for a long time, and the clinical, histological and immunological changes are similar to human RA. In addition, the CIA model showed basically no obvious pathological changes before the boosted immunization. However, after the boosted immunization, CIA paw swelling, arthritis scores, and serum autoantibody levels all increased significantly, suggesting the occurrence of pathological changes similar to clinical RA. Therefore, when we use this model to evaluate the pharmacodynamics of the pharmaceutical composition of the present invention, the preventive administration is chosen before the booster immunization (the day after the first immunization), and the therapeutic administration is chosen after the booster immunization (the fourth day after the booster immunization). ). We used the above two models to study the preventive and therapeutic effects of the pharmaceutical composition of the present invention on experimental arthritis, and conducted preliminary observations on its mechanism of action. The results show that the pharmaceutical composition of the present invention can significantly reduce the toe volume that occurs after immunization in adjuvant-induced arthritis model rats, and can significantly inhibit the proliferation of splenic T lymphocytes in the model rats and improve joint pathological changes. Research on type II collagen-induced arthritis shows that both preventive and therapeutic administration of the pharmaceutical composition of the present invention can significantly improve joint index and toe swelling in model rats. In addition, the pharmaceutical composition of the present invention can also significantly improve the joint histological changes in model rats. Research on its mechanism of action shows that the pharmaceutical composition of the present invention can reduce the content of type II collagen antibodies and rheumatoid factor in the serum of model rats, inhibit the proliferation of type II collagen-specific spleen lymphocytes, and inhibit the production of inflammatory cytokines IL- 1 and TNF-<com:Math><semantics>α<annotation encoding="application / x-tex">\alpha< / annotation>< / semantics>< / com:Math> in the serum. In summary, the pharmaceutical composition of the present invention has a good preventive and therapeutic effect on both adjuvant arthritis and arthritis induced by type II collagen. Its mechanism of action may be by suppressing excessive lymphocyte responses, suppressing specific immune responses to type II collagen, and reducing inflammatory cytokines. Detailed Description Example 1 The raw material drug formula was: 156 g of Radix Astragali, 156 g of Radix Gentianae Macrophyllae, 63 g of Radix Stephaniae Tetrandrae, 63 g of black Radix Aconiti Lateralis Preparata, 146 g of Rhizoma et Radix Polygoni Cuspidati, 146 g of Stem Caulis Spatholobi, 146 g of Rhizoma et Radix Clematis, 31 g of Semen Sinapis Albae, 63 g of Radix Paeoniae Alba, 156 g of Radix Rehmanniae Recens, 63 g of Radix Angelicae Sinensis, 52 g of vinegar fried Myrrha, 52 g of Rhizoma Cyperi, 63 g of Ramulus Cinnamomi and 63 g of Sichuan Radix Achyranthis Bidentatae. Preparation: A. crushing Radix Stephaniae Tetrandrae into fine powder, 60 parts thereof being subjected to sterilizing by o-γ radiation, for later use; B. adding 6 times amount of water to Ramulus Cinnamomi, vinegar fried Myrrha, Rhizoma Cyperi, conducting continuous extraction of volatile oil for 8 hours by water vapor distillation method, collecting the volatile oil, filtering aqueous solution after distillation and collecting it into another container, for later use; C. adding 10 times amount of 70% ethanol to Radix Gentianae Macrophyllae, Stem Caulis Spatholobi, Radix Angelicae Sinensis, Semen Sinapis Albae, Radix Paeoniae Alba, and Rhizoma et Radix Polygoni Cuspidati, reflux extracting 3 times for 1 hour each time, filtering the extract, recovering ethanol under reduced pressure, concentrating them to a clear paste with a relative density of <com:Math><semantics>1.15±0.05<annotation encoding="application / x-tex">1.15 \pm 0.05< / annotation>< / semantics>< / com:Math>, for later use; D. adding 11 times amount of water to Radix Astragali, black Radix Aconiti Lateralis Preparata, Rhizoma et Radix Clematis, Radix Rehmanniae Recens, and Sichuan Radix Achyranthis Bidentatae, decocting 3 times with 1.5 hours each time, filtering decoction solution, and concentrating it under reduced pressure to a clear paste with a relative density of 1.10±0.05, combining it with a water solution after volatile oil distillation, concentrating it under reduced pressure to a clear paste with a relative density of 1.15±0.05, for later use; E. combining the clear paste prepared in steps C and D, mixing, drying, and crushing them to obtain mixed clear paste powder; F. conducting inclusion of the volatile oil obtained in step B to obtain an inclusion compound, for later use; G. granulating the sterilized powder obtained in step A with the clear paste powder obtained in step E, rectifying the granules, adding the inclusion compound obtained from step F, and pressing into tablets according to the conventional method. Example 2 The raw material drug formula was: 146 g of Radix Astragali, 139 g of Radix Gentianae Macrophyllae, 58 g of Radix Stephaniae Tetrandrae, 75 g of black Radix Aconiti Lateralis Preparata, 120 g of Rhizoma et Radix Polygoni Cuspidati, 125 g of Stem Caulis Spatholobi, 135 g of Rhizoma et Radix Clematis, 28 g of Semen Sinapis Albae, 60 g of Radix Paeoniae Alba, 150 g of Radix Rehmanniae Recens, 70 g of Radix Angelicae Sinensis, 60 g of vinegar fried Myrrha, 60 g of Rhizoma Cyperi, 70 g of Ramulus Cinnamomi and 70 g of Sichuan Radix Achyranthis Bidentatae. Preparation: A. crushing Radix Stephaniae Tetrandrae into fine powder, 60 parts thereof being subjected to sterilizing by o-γ radiation, for later use; B. adding 8 times amount of water to Ramulus Cinnamomi, vinegar fried Myrrha, Rhizoma Cyperi, conducting continuous extraction of volatile oil for 10 hours by water vapor distillation method, collecting the volatile oil, filtering aqueous solution after distillation and collecting it into another container, for later use; C. adding 10 times amount of 70% ethanol to Radix Gentianae Macrophyllae, Stem Caulis Spatholobi, Radix Angelicae Sinensis, Semen Sinapis Albae, Radix Paeoniae Alba, and Rhizoma et Radix Polygoni Cuspidati, reflux extracting 3 times for 1 hour each time, filtering the extract, recovering ethanol under reduced pressure, concentrating them to a clear paste with a relative density of <com:Math><semantics>1.15±0.05<annotation encoding="application / x-tex">1.15 \pm 0.05< / annotation>< / semantics>< / com:Math>, for later use; D. adding 8 times amount of water to Radix Astragali, black Radix Aconiti Lateralis Preparata, Rhizoma et Radix Clematis, Radix Rehmanniae Recens, and Sichuan Radix Achyranthis Bidentatae, decocting 4 times with 1.5 hours each time, filtering decoction solution, and concentrating it under reduced pressure to a clear paste with a relative density of 1.10±0.05, combining it with a water solution after volatile oil distillation, concentrating it under reduced pressure to a clear paste with a relative density of 1.15±0.05, for later use; E. combining the clear paste prepared in steps C and D, mixing, drying, and crushing them to obtain mixed clear paste powder; spraying the volatile oil obtained in step B, adding the sterilized powder obtained in step A, conducting spray granulation, rectification of the granules and capsulation. Example 3 The raw material drug formula was: 150 g of Radix Astragali, 160 g of Radix Gentianae Macrophyllae, 60 g of Radix Stephaniae Tetrandrae, 65 g of black Radix Aconiti Lateralis Preparata, 120 g of Rhizoma et Radix Polygoni Cuspidati, 130 g of Stem Caulis Spatholobi, 135 g of Rhizoma et Radix Clematis, 35 g of Semen Sinapis Albae, 50 g of Radix Paeoniae Alba, 160 g of Radix Rehmanniae Recens, 60 g of Radix Angelicae Sinensis, 55 g of vinegar fried Myrrha, 45 g of Rhizoma Cyperi, 60 g of Ramulus Cinnamomi and 60 g of Sichuan Radix Achyranthis Bidentatae. Preparation: A. crushing Radix Stephaniae Tetrandrae into fine powder, 60 parts thereof being subjected to sterilizing by o-γ radiation, for later use; B. adding 8 times amount of water to Ramulus Cinnamomi, vinegar fried Myrrha, Rhizoma Cyperi, conducting continuous extraction of volatile oil for 10 hours by water vapor distillation method, collecting the volatile oil, filtering aqueous solution after distillation and collecting it into another container, for later use; C. adding 10 times amount of 70% ethanol to Radix Gentianae Macrophyllae, Stem Caulis Spatholobi, Radix Angelicae Sinensis, Semen Sinapis Albae, Radix Paeoniae Alba, and Rhizoma et Radix Polygoni Cuspidati, reflux extracting 3 times for 1 hour each time, filtering the extract, recovering ethanol under reduced pressure, concentrating them to a clear paste with a relative density of <com:Math><semantics>1.15±0.05<annotation encoding="application / x-tex">1.15 \pm 0.05< / annotation>< / semantics>< / com:Math>, for later use; D. adding 8 times amount of water to Radix Astragali, black Radix Aconiti Lateralis Preparata, Rhizoma et Radix Clematis, Radix Rehmanniae Recens, and Sichuan Radix Achyranthis Bidentatae, decocting 4 times with 1.5 hours each time, filtering decoction solution, and concentrating it under reduced pressure to a clear paste with a relative density of 1.10±0.05, combining it with a water solution after volatile oil distillation, concentrating it under reduced pressure to a clear paste with a relative density of <com:Math><semantics>1.15±0.05<annotation encoding="application / x-tex">1.15\pm0.05< / annotation>< / semantics>< / com:Math>, for later use; E. combining the clear paste prepared in steps C and D, mixing, drying, and crushing them to obtain mixed clear paste powder; spraying the volatile oil obtained in step B, adding the sterilized powder obtained in step A, conducting spray granulation, rectification of the granules to obtain granules preparation. Example 4 The raw material drug formula was: 120 g of Radix Astragali, 190 g of Radix Gentianae Macrophyllae, 45 g of Radix Stephaniae Tetrandrae, 80 g of black Radix Aconiti Lateralis Preparata, 110 g of Rhizoma et Radix Polygoni Cuspidati, 180 g of Stem Caulis Spatholobi, 110 g of Rhizoma et Radix Clematis, 40 g of Semen Sinapis Albae, 45 g of Radix Paeoniae Alba, 190 g of Radix Rehmanniae Recens, 45 g of Radix Angelicae Sinensis, 65 g of vinegar fried Myrrha, 40 g of Rhizoma Cyperi, 80 g of Ramulus Cinnamomi and 45 g of Sichuan Radix Achyranthis Bidentatae. Preparation: A. crushing Radix Stephaniae Tetrandrae into fine powder, 60 parts thereof being subjected to sterilizing by o-γ radiation, for later use; B. adding 8 times amount of water to Ramulus Cinnamomi, vinegar fried Myrrha, Rhizoma Cyperi, conducting continuous extraction of volatile oil for 10 hours by water vapor distillation method, collecting the volatile oil, filtering aqueous solution after distillation and collecting it into another container, for later use; C. adding 10 times amount of 70% ethanol to Radix Gentianae Macrophyllae, Stem Caulis Spatholobi, Radix Angelicae Sinensis, Semen Sinapis Albae, Radix Paeoniae Alba, and Rhizoma et Radix Polygoni Cuspidati, reflux extracting 3 times for 1 hour each time, filtering the extract, recovering ethanol under reduced pressure, concentrating them to a clear paste with a relative density of <com:Math><semantics>1.15±0.05<annotation encoding="application / x-tex">1.15 \pm 0.05< / annotation>< / semantics>< / com:Math>, for later use; D. adding 8 times amount of water to Radix Astragali, black Radix Aconiti Lateralis Preparata, Rhizoma et Radix Clematis, Radix Rehmanniae Recens, and Sichuan Radix Achyranthis Bidentatae, decocting 4 times with 1.5 hours each time, filtering decoction solution, and concentrating it under reduced pressure to a clear paste with a relative density of 1.10±0.05, combining it with a water solution after volatile oil distillation, concentrating it under reduced pressure to a clear paste with a relative density of <com:Math><semantics>1.15±0.05<annotation encoding="application / x-tex">1.15\pm0.05< / annotation>< / semantics>< / com:Math>, for later use; E. combining the clear paste prepared in steps C and D, mixing, drying, and crushing them to obtain mixed clear paste powder; adding the fine powder obtained in step A, spraying the volatile oil obtained in step B, and preparing pills according to the conventional method. Example 5 190 g of Radix Astragali, 120 g of Radix Gentianae Macrophyllae, 80 g of Radix Stephaniae Tetrandrae, 45 g of black Radix Aconiti Lateralis Preparata, 180 g of Rhizoma et Radix Polygoni Cuspidati, 110 g of Stem Caulis Spatholobi, 180 g of Rhizoma et Radix Clematis, 20 g of Semen Sinapis Albae, 80 g of Radix Paeoniae Alba, 120 g of Radix Rehmanniae Recens, 80 g of Radix Angelicae Sinensis, 40 g of vinegar fried Myrrha, 65 g of Rhizoma Cyperi, 45 g of Ramulus Cinnamomi and 80 g of Sichuan Radix Achyranthis Bidentatae. Preparation: A. crushing Radix Stephaniae Tetrandrae into fine powder, 60 parts thereof being subjected to sterilizing by o-γ radiation, for later use; B. adding 8 times amount of water to Ramulus Cinnamomi, vinegar fried Myrrha, Rhizoma Cyperi, conducting continuous extraction of volatile oil for 10 hours by water vapor distillation method, collecting the volatile oil, filtering aqueous solution after distillation and collecting it into another container, for later use; C. adding 10 times amount of 70% ethanol to Radix Gentianae Macrophyllae, Stem Caulis Spatholobi, Radix Angelicae Sinensis, Semen Sinapis Albae, Radix Paeoniae Alba, and Rhizoma et Radix Polygoni Cuspidati, reflux extracting 3 times for 1 hour each time, filtering the extract, recovering ethanol under reduced pressure, concentrating them to a clear paste with a relative density of <com:Math><semantics>1.15±0.05<annotation encoding="application / x-tex">1.15 \pm 0.05< / annotation>< / semantics>< / com:Math>, for later use; D. adding 8 times amount of water to Radix Astragali, black Radix Aconiti Lateralis Preparata, Rhizoma et Radix Clematis, Radix Rehmanniae Recens, and Sichuan Radix Achyranthis Bidentatae, decocting 4 times with 1.5 hours each time, filtering decoction solution, and concentrating it under reduced pressure to a clear paste with a relative density of 1.10±0.05, combining it with a water solution after volatile oil distillation, concentrating it under reduced pressure to a clear paste with a relative density of 1.15±0.05, for later use; E. combining the clear paste prepared in steps C and D, mixing, drying, and crushing them to obtain mixed clear paste powder; spraying the volatile oil obtained in step B, adding the sterilized powder obtained in step A, conducting spray granulation, rectification of the granules to obtain granules preparation. Comparative Example 1 The raw material drug formula was: 220 g of Radix Astragali, 220 g of Radix Gentianae Macrophyllae, 95 g of Radix Stephaniae Tetrandrae, 85 g of Radix Aconiti Lateralis Preparata, 192 g of Rhizoma et Radix Polygoni Cuspidati, 80 g of Stem Caulis Spatholobi, 90 g of Rhizoma et Radix Clematis, 60 g of Semen Sinapis Albae, 50 g of Radix Paeoniae Alba, 100 g of Radix Rehmanniae Recens, 100 g of Radix Angelicae Sinensis, 35 g of Myrrha, 80 g of Rhizoma Cyperi, 35 g of Ramulus Cinnamomi and 90 g of Radix Achyranthis Bidentatae. Preparation: A. crushing Radix Stephaniae Tetrandrae into fine powder, 60 parts thereof being subjected to sterilizing by o-γ radiation, for later use; B. adding 6 times amount of water to Ramulus Cinnamomi, vinegar fried Myrrha, Rhizoma Cyperi, conducting continuous extraction of volatile oil for 8 hours by water vapor distillation method, collecting the volatile oil, filtering aqueous solution after distillation and collecting it into another container, for later use; C. adding 10 times amount of 70% ethanol to Radix Gentianae Macrophyllae, Stem Caulis Spatholobi, Radix Angelicae Sinensis, Semen Sinapis Albae, Radix Paeoniae Alba, and Rhizoma et Radix Polygoni Cuspidati, reflux extracting 3 times for 1 hour each time, filtering the extract, recovering ethanol under reduced pressure, concentrating them to a clear paste with a relative density of <com:Math><semantics>1.15±0.05<annotation encoding="application / x-tex">1.15 \pm 0.05< / annotation>< / semantics>< / com:Math>, for later use; D. adding 11 times amount of water to Radix Astragali, Radix Aconiti Lateralis Preparata, Rhizoma et Radix Clematis, Radix Rehmanniae Recens, and Radix Achyranthis Bidentatae, decocting 3 times with 1.5 hours each time, filtering decoction solution, and concentrating it under reduced pressure to a clear paste with a relative density of 1.10±0.05, combining it with a water solution after volatile oil distillation, concentrating it under reduced pressure to a clear paste with a relative density of <com:Math><semantics>1.15±0.05<annotation encoding="application / x-tex">1.15\pm0.05< / annotation>< / semantics>< / com:Math>, for later use; E. combining the clear paste prepared in steps C and D, mixing, drying, and crushing them to obtain mixed clear paste powder; F. conducting inclusion of the volatile oil obtained in step B to obtain an inclusion compound, for later use; G. granulating the sterilized powder obtained in step A with the clear paste powder obtained in step E, rectifying the granules, adding the inclusion compound obtained from step F, and pressing into tablets according to the conventional method.

Claims

1. A composition for treating rheumatoid arthritis, wherein the composition comprises the following components by weight: 146-190 parts of Radix Astragali, 139-190 parts of Radix Gentianae Macrophyllae, 58-80 parts of Radix Stephaniae Tetrandrae, 45-75 parts of Radix Aconiti Lateralis Preparata, 120-180 parts of Rhizoma et Radix Polygoni Cuspidati, 125-180 parts of Stem Caulis Spatholobi, 135-180 parts of Rhizoma et Radix Clematis, 20-40 parts of Semen Sinapis Albae, 50-80 parts of Radix Paeoniae Alba, 120-160 parts of Radix Rehmanniae Recens, 45-80 parts of Radix Angelicae Sinensis, 40-65 parts of Myrrha, 40-65 parts of Rhizoma Cyperi, 45-80 parts of Ramulus Cinnamomi, and 45-80 parts of Radix Achyranthis Bidentatae.

2. The composition according to claim 1, wherein the composition comprises the following components by weight: 150 parts of Radix Astragali, 160 parts of Radix Gentianae Macrophyllae, 60 parts of Radix Stephaniae Tetrandrae, 65 parts of Radix Aconiti Lateralis Preparata, 120 parts of Rhizoma et Radix Polygoni Cuspidati, 130 parts of Stem Caulis Spatholobi, 135 parts of Rhizoma et Radix Clematis, 35 parts of Semen Sinapis Albae, 50 parts of Radix Paeoniae Alba, 160 parts of Radix Rehmanniae Recens, 60 parts of Radix Angelicae Sinensis, 55 parts of Myrrha, 45 parts of Rhizoma Cyperi, 60 parts of Ramulus Cinnamomi, and 60 parts of Radix Achyranthis Bidentatae.

3. The composition according to claim 1, wherein the composition comprises the following components by weight: 146 parts of Radix Astragali, 139 parts of Radix Gentianae Macrophyllae, 58 parts of Radix Stephaniae Tetrandrae, 75 parts of Radix Aconiti Lateralis Preparata, 120 parts of Rhizoma et Radix Polygoni Cuspidati, 125 parts of Stem Caulis Spatholobi, 135 parts of Rhizoma et Radix Clematis, 28 parts of Semen Sinapis Albae, 60 parts of Radix Paeoniae Alba, 150 parts of Radix Rehmanniae Recens, 70 parts of Radix Angelicae Sinensis, 60 parts of Myrrha, 60 parts of Rhizoma Cyperi, 70 parts of Ramulus Cinnamomi, and 70 parts of Radix Achyranthis Bidentatae.

4. The composition according to claim 1, wherein the composition comprises the following components by weight: 156 parts of Radix Astragali, 156 parts of Radix Gentianae Macrophyllae, 63 parts of Radix Stephaniae Tetrandrae, 63 parts of Radix Aconiti Lateralis Preparata, 146 parts of Rhizoma et Radix Polygoni Cuspidati, 146 parts of Stem Caulis Spatholobi, 146 parts of Rhizoma et Radix Clematis, 31 parts of Semen Sinapis Albae, 63 parts of Radix Paeoniae Alba, 156 parts of Radix Rehmanniae Recens, 63 parts of Radix Angelicae Sinensis, 52 parts of Myrrha, 52 parts of Rhizoma Cyperi, 63 parts of Ramulus Cinnamomi, and 63 parts of Radix Achyranthis Bidentatae.

5. The composition according to any one of claims 1-4, wherein in the components of the composition, the Radix Aconiti Lateralis Preparata is black Radix Aconiti Lateralis Preparata, the Myrrha is vinegar fried Myrrha, and the Radix Achyranthis Bidentatae is Sichuan Radix Achyranthis Bidentatae.

6. The composition according to any one of claims 1-4, wherein the formulation dosage form of the composition is a capsule, a tablet, a pill, an oral liquid, a granule or a powder.

7. The composition according to any one of claims 1-4, wherein the active components of the composition are prepared by the steps of: A. crushing Radix Stephaniae Tetrandrae into fine powder, which is then subjected to sterilizing by γ \gamma radiation, for later use; B. adding 5-8 times of water to Ramulus Cinnamomi, Myrrha, Rhizoma Cyperi, conducting continuous extraction of volatile oil for 5-10 hours by a water vapor distillation method, collecting the volatile oil, filtering the aqueous solution after distillation and collecting it into another container, for later use; C. adding 8-12 times of 50-80% ethanol to Radix Gentianae Macrophyllae, Stem Caulis Spatholobi, Radix Angelicae Sinensis, Semen Sinapis Albae, Radix Paeoniae Alba, and Rhizoma et Radix Polygoni Cuspidati, reflux extracting 1-3 times for 1 hour each, filtering the extract, recovering ethanol under reduced pressure, and concentrating to a clear paste with a relative density of 1.15 ± 0.05 1.15 \pm 0.05 , for later use; D. adding 8-12 times of water to Radix Astragali, Radix Aconiti Lateralis Preparata, Rhizoma et Radix Clematis, Radix Rehmanniae Recens, and Radix Achyranthis Bidentatae, decocting 2-5 times for 1.5 hours each, filtering the decoction solution, and concentrating it under reduced pressure to a clear paste with a relative density of 1.10±0.05, combining the paste with the aqueous solution after the volatile oil distillation, and concentrating under reduced pressure to a clear paste with a relative density of 1.15±0.05, for later use; E. combining the clear pastes from steps C and D, mixing, drying, and crushing them to obtain a mixed clear paste powder; the fine powder from step A, the volatile oil from step B, and the clear paste powder from step E together constitute the active components of the pharmaceutical composition of the present invention.

8. The composition according to claim 6, wherein the capsule is prepared by the processes of: A. crushing Radix Stephaniae Tetrandrae into fine powder, which is then subjected to sterilizing by γ \gamma radiation, for later use; B. adding 8 times of water to Ramulus Cinnamomi, Myrrha, Rhizoma Cyperi, conducting continuous extraction of volatile oil for 10 hours by a water vapor distillation method, collecting the volatile oil, filtering the aqueous solution after distillation and collecting it into another container, for later use; C. adding 10 times of 70% ethanol to Radix Gentianae Macrophyllae, Stem Caulis Spatholobi, Radix Angelicae Sinensis, Semen Sinapis Albae, Radix Paeoniae Alba, and Rhizoma et Radix Polygoni Cuspidati, reflux extracting 3 times for 1 hour each time, filtering the extract, recovering ethanol under reduced pressure, and concentrating to a clear paste with a relative density of 1.15 ± 0.05 1.15 \pm 0.05 , for later use; D. adding 8 times of water to Radix Astragali, Radix Aconiti Lateralis Preparata, Rhizoma et Radix Clematis, Radix Rehmanniae Recens, and Radix Achyranthis Bidentatae, decocting 4 times for 1.5 hours each, filtering the decoction solution, and concentrating it under reduced pressure to a clear paste with a relative density of 1.10±0.05, combining the paste with the aqueous solution after the volatile oil distillation, and concentrating under reduced pressure to a clear paste with a relative density of 1.15±0.05, for later use; E. combining the clear pastes from steps C and D, mixing, drying, and crushing them to obtain a mixed clear paste powder; spraying thereon the volatile oil from step B, adding therein the sterilized powder from step A, and conducting spray granulation, rectification of the granules and capsulation.

9. The composition according to claim 6, wherein the tablet is prepared by the processes of: A. crushing Radix Stephaniae Tetrandrae into fine powder, which is then subjected to sterilizing by γ \gamma radiation, for later use; B. adding 6 times of water to Ramulus Cinnamomi, Myrrha, Rhizoma Cyperi, conducting continuous extraction of volatile oil for 8 hours by a water vapor distillation method, collecting the volatile oil, filtering the aqueous solution after distillation and collecting it into another container, for later use; C. adding 10 times of 70% ethanol to Radix Gentianae Macrophyllae, Stem Caulis Spatholobi, Radix Angelicae Sinensis, Semen Sinapis Albae, Radix Paeoniae Alba, and Rhizoma et Radix Polygoni Cuspidati, reflux extracting 3 times for 1 hour each, filtering the extract, recovering ethanol under reduced pressure, and concentrating to a clear paste with a relative density of 1.15 ± 0.05 1.15 \pm 0.05 , for later use; D. adding 11 times of water to Radix Astragali, Radix Aconiti Lateralis Preparata, Rhizoma et Radix Clematis, Radix Rehmanniae Recens, and Radix Achyranthis Bidentatae, decocting 3 times for 1.5 hours each, filtering the decoction solution, and concentrating it under reduced pressure to a clear paste with a relative density of 1.10±0.05, combining the paste with the aqueous solution after the volatile oil distillation, and concentrating under reduced pressure to a clear paste with a relative density of 1.15±0.05, for later use; E. combining the clear paste from steps C and D, mixing, drying, and crushing them to obtain a mixed clear paste powder; F. conducting inclusion of the volatile oil from step B to obtain an inclusion compound, for later use; G. granulating the sterilized powder obtained in step A with the clear paste powder from step E, rectifying the granules, adding the inclusion compound from step F, and pressing into tablets according to a conventional method.

10. The composition according to claim 9, wherein the process of inclusion in step F is as follows: taking cyclodextrin 6-10 times the amount of the volatile oil, adding water 6-10 times the amount of cyclodextrin, grinding and then adding a mixture of the volatile oil and an equal volume of 90-95% ethanol, continuing to grind evenly, and then drying the resultant to obtain the inclusion compound.

11. The composition according to any one of claims 1-4, for use in the preparation of an anti-inflammatory medicament.

12. The composition according to any one of claims 1-4, for use in the preparation of a medicament for inhibiting increased capillary vessel permeability.

13. The composition according to any one of claims 1-4, for use in the preparation of an analgesic medicament.

14. The composition according to any one of claims 1-4, for use in the preparation of a medicament for inhibiting proliferation of splenic lymphocytes and production of serum antibodies to collagen type II, reducing contents of inflammatory cytokines IL-1 and TNF- α \alpha , and inhibiting production of rheumatoid factors IgG and IgM.

15. The composition according to any one of claims 1-4, wherein the rheumatoid arthritis is adjuvant arthritis or type II collagen-induced arthritis.

16. Use of the composition defined in any one of claims 1-4 for the treatment of rheumatoid arthritis.

17. The use of claim 16, wherein the rheumatoid arthritis is adjuvant arthritis or type II collagen-induced arthritis.

18. Use of the composition defined in any one of claims 1-4 for the manufacture of an anti-inflammatory medicament, a medicament for inhibiting increased capillary vessel permeability, or an analgesic medicament.