Application of Guiqi Huoxue preparation in preparation of drugs for treating arteriosclerosis

Abstract

The application of Guqi Huoxue preparation in the preparation of drugs for treating arteriosclerosis. The application belongs to the technical field of traditional Chinese medicine, and discloses a new use of Guqi Huoxue preparation, in particular, the use of Guqi Huoxue preparation in the preparation of drugs for treating arteriosclerosis. The Guqi Huoxue preparation is mainly prepared from Huangqi, Danggui, Baishao, Heshouwu, Gouqi, Suanzaoren, Lurong, Gushugu, Weilingxian, Tougucao, Mosha, Gegen and Chuanxiong. Modern pharmacological experiments show that the Guqi Huoxue preparation has a good preventive or therapeutic effect on arteriosclerosis, can significantly reduce arteriosclerosis plaques, effectively inhibit the progress of arteriosclerosis, and obviously relieve the symptoms of arteriosclerosis.

Description

TECHNICAL FIELD

[0001] The application belongs to the technical field of traditional Chinese medicine, and particularly relates to application of a Guipi Huoxue preparation in atherosclerosis drugs, especially in cerebral atherosclerosis and carotid atherosclerosis drugs. BACKGROUND

[0002] Atherosclerosis (AS) is a progressive pathological process characterized by intimal hyperplasia, hardening and decreased elasticity of the arterial wall, leading to stenosis of the lumen, abnormal vasodilation and vasodilation, and is the pathological basis of coronary heart disease, stroke and other cardiovascular diseases. According to the different lesion sites, it can be divided into aortic atherosclerosis, coronary atherosclerosis, carotid atherosclerosis, cerebral atherosclerosis, renal atherosclerosis and mesenteric atherosclerosis.

[0003] Cerebral arteriosclerosis (CAS) is a kind of arteriosclerosis occurring in the brain, which is part of systemic arteriosclerosis, and is also the main basis for acute cerebral blood circulation, especially cerebral ischemia, and is a general term for cerebral arterial wall degeneration and hardening caused by various factors. It includes non-acute, diffuse brain tissue changes and neurological dysfunction caused by arterial wall degeneration such as cerebral atherosclerosis, small artery sclerosis and glass-like change.

[0004] Cerebral arteriosclerosis is a kind of clinical cerebrovascular disease, and the main symptoms are dizziness, headache, tinnitus, memory loss, insomnia and the like, and severe cases can be accompanied by behavior or personality changes, even anxiety and depression, which seriously affect the quality of life of patients. Cerebral arteriosclerosis is common and frequently occurring, and is prone to occur in the elderly.

[0005] There is no specific treatment for cerebral arteriosclerosis in Western medicine, and the efficacy is poor. The main treatment is prevention and treatment of atherosclerosis, as well as increasing cerebral blood supply, improving cerebral circulation, and symptomatic treatment of mental and neurological symptoms. Common drugs include brain activator piracetam, dihydroergotoxine mesylate, calcium channel antagonists such as flunarizine and nitrendipine, and vasodilator drugs such as benzazoline and phenoxybenzamine. Traditional Chinese medicine has significant advantages and efficacy in the treatment of chronic cerebrovascular disease, and people hope to use traditional Chinese medicine to treat cerebral arteriosclerosis.

[0006] Traditional Chinese medicine does not record "cerebral arteriosclerosis" as a specific disease. Based on clinical characteristics and its progression, it is often categorized under terms such as "dizziness," "headache," "insomnia," "forgetfulness," and "dementia." Cerebral arteriosclerosis is located in the brain, involving the heart, liver, spleen, and kidneys. Its pathogenesis is characterized by deficiency, blood stasis, and phlegm. Deficiency refers to the underlying deficiency, such as insufficient qi and blood, and depletion of kidney essence; phlegm and blood stasis are the superficial excesses, representing phlegm turbidity and blood stasis that obstruct the brain's collaterals. Deficiency, blood stasis, and phlegm obstruction are the fundamental pathogenesis of cerebral arteriosclerosis, with mutual obstruction of phlegm and blood stasis being the key pathological aspect. Traditional Chinese medicine clinically classifies arteriosclerosis based on its specific pathogenesis, often dividing it into several patterns: kidney essence deficiency, liver yang hyperactivity, qi and blood deficiency, phlegm turbidity obstruction, or mutual obstruction of phlegm and blood stasis. Commonly used formulas in traditional Chinese medicine for treating cerebral arteriosclerosis include those for promoting blood circulation, nourishing yin, tonifying the kidneys, nourishing the liver, suppressing yang, replenishing qi, and resolving phlegm.

[0007] Carotid atherosclerosis (CAS) is a disease characterized by narrowing of the lumen of one or both carotid arteries, leading to circulatory disorders. Its main pathological changes include vascular thickening, lipid deposition, and plaque formation. CAS serves as an important observational window into systemic arteriosclerosis. The occurrence and development of CAS foreshadow the progression of cardiovascular and cerebrovascular diseases and is also a significant contributing factor to these diseases.

[0008] Carotid artery sclerosis is generally considered a condition in Traditional Chinese Medicine (TCM) characterized by deficiency of the root and excess of the branch, or a mixture of deficiency and excess, with phlegm, blood stasis, and toxins permeating its entire course. Located in the blood vessels of the neck, prolonged stagnation of phlegm obstructs the flow of qi and blood, leading to sluggish blood circulation. Over time, these toxins damage the blood vessels, eventually causing atherosclerotic plaques. Western medicine often treats carotid artery sclerosis with statins, but long-term use of statins can increase liver and kidney damage and worsen systemic circulatory disorders.

[0009] Traditional Chinese medicine (TCM) has accumulated rich experience in treating arteriosclerosis due to its advantages such as multiple components, multiple targets, multiple pathways of action, and fewer toxic side effects. Prepared Chinese medicines, as one of the main forms of TCM treatment for arteriosclerosis, are an indispensable part of TCM's unique therapeutic approach. Therefore, exploring more TCM treatments for arteriosclerosis is of paramount importance.

[0010] Guiqi Huoxue Capsules, approved by the State Drug Administration (Z20090686) and manufactured by Lunan Houpu Pharmaceutical Co., Ltd., have the effects of invigorating qi and tonifying the kidneys, promoting blood circulation and unblocking collaterals. They are used for cervical spondylosis (nerve root type and mixed type mainly of nerve root type) with liver and kidney deficiency, qi deficiency and blood stasis syndrome, characterized by neck pain and heaviness, shoulder and back pain, numbness in the arms, weakness and atrophy of the limbs, dizziness, dark red or pale tongue with ecchymosis, thin white coating, and deep, weak, or deep, wiry, and hesitant pulse. However, the effects of Guiqi Huoxue Capsules on arteriosclerosis have not yet been reported. Summary of the Invention

[0011] In order to enrich the medication selection for treating arteriosclerosis in clinic, the purpose of the present application is to provide a new use of Guqihuoxue preparation, especially in the preparation of a drug for treating arteriosclerosis.

[0012] The application of Guqihuoxue preparation in the preparation of a drug for treating arteriosclerosis.

[0013] Preferably, the arteriosclerosis is cerebral arteriosclerosis or carotid arteriosclerosis.

[0014] Preferably, the cerebral arteriosclerosis or carotid arteriosclerosis is of the type of qi deficiency and blood stasis, the type of qi and blood deficiency, the type of phlegm turbidity obstruction or the type of phlegm and blood stasis obstruction.

[0015] Further preferably, the cerebral arteriosclerosis or carotid arteriosclerosis is of the type of qi deficiency and blood stasis.

[0016] Preferably, the Guqihuoxue preparation is Guqihuoxue capsules.

[0017] Modern medical research shows that Guqihuoxue capsules can reduce the serum TC, TG and LDL-C of carotid arteriosclerosis rats, can significantly inhibit the levels of SDF-1, CX-CR4 and VEGF of rats, and then reduce the degree of carotid arteriosclerosis plaque of rats and relieve the symptoms of arteriosclerosis.

[0018] Guqihuoxue capsules can reduce blood viscosity, dilate blood vessels, improve blood flow, significantly improve lipid metabolism disorder, regulate the levels of NO, ET, TXB2 and 6-keto-PGF 1α , and then regulate vascular function, significantly reduce the risk degree of cerebral arteriosclerosis, inhibit the progress of cerebral arteriosclerosis and relieve the symptoms of cerebral arteriosclerosis.

[0019] Clinical practice observation and animal experiments show that Guqihuoxue capsules of the present application have good prevention or treatment effect on cerebral arteriosclerosis and carotid arteriosclerosis. DETAILED DESCRIPTION

[0020] According to the above content of the present application, according to the ordinary technical knowledge and common means in the art, other various forms of modification, replacement or change can be made without departing from the above basic technical idea of the present application.

[0021] The above content of the present application is further explained in detail through the specific embodiments in the form of examples. However, it should not be understood that the above subject matter of the present application is limited to the following examples. Any technology realized based on the above content of the present application belongs to the scope of the present application.

[0022] Experimental Example 1: Effect of Guqihuoxue Capsules on Carotid Arteriosclerosis Model Rats

[0023] 1 Experimental materials

[0024] 1.1 Experimental animals

[0025] 42 healthy clean adult male Wistar rats with a body weight of 200 ± 20 g were provided by Lu'nan Pharmaceutical Group Co., Ltd. with license SYXK(Lu)2018-0008 and were bred in the pharmacology center of Lu'nan Pharmaceutical Group. All rats were adaptively cultured with ordinary feed for 1 week.

[0026] 1.2 Reagents, drugs and instruments

[0027] TRIzol reagent, Invitrogen, USA; total cholesterol TC, triglyceride TG and low-density lipoprotein cholesterol LDL-C assay kit, Nanjing Jianshen Biological Engineering Institute; SDF-1 (serum stromal cell-derived factor-1), CXCR4 (chemotactic receptor-4), VEGF (vascular endothelial growth factor) Elisa kit, Wuhan Biode Company Limited. Guqia Huoxue Capsules, State Drug Approval Z20090686, Lu'nan Hupu Pharmaceutical Co., Ltd. Atorvastatin calcium tablets, State Drug Approval HJ20170215, Pfizer Pharmaceutical Co., Ltd. Automatic biochemical analyzer, Toshiba, Japan. Beijing Pucheng multifunctional enzyme marker PT-3502A.

[0028] 2 Experimental methods

[0029] 2.1 Animal grouping, modeling and administration

[0030] Ten rats were randomly selected as the blank control group and were fed with ordinary feed. The remaining 32 rats were fed with high-fat feed, 30 g / kg of high-fat feed was taken every day (high-fat feed contained 81.3% basic feed, 3% cholesterol, 0.5% sodium cholate, 0.2% propylthiouracil, 5% white sugar and 10% lard), and the feeding was continued for 12 weeks. Two rats fed with high-fat feed for 12 weeks were dissected, and their carotid arteries were taken for pathological section to confirm the success of modeling. The rats in each modeling group were randomly divided into three groups, namely the model control group, the positive control group and the Guqia Huoxue Capsule group, with 10 rats in each group. The blank control group was continuously fed with ordinary feed for 4 weeks; the model control group was fed with high-fat feed at 30 g / kg per day for 4 weeks; the positive control group was fed with high-fat feed at 30 g / kg per day and orally administered with atorvastatin calcium tablets at 0.9 mg / kg / d for 4 weeks; the Guqia Huoxue Capsule group was fed with high-fat feed at 30 g / kg per day and orally administered with Guqia Huoxue Capsules at 0.45 g / kg / d for 4 weeks.

[0031] 2.2 Index determination

[0032] 2.2.1 Detection of TC, TG and LDL-C

[0033] After 16 weeks of feeding, 5 mL of fasting blood was taken from the surgical side of the common carotid artery of each group of rats, and the serum was obtained after centrifugation. The TC, TG, and LDL-C levels were determined by chemical enzyme method using a fully automatic biochemical analyzer.

[0034] 2.2.2 Determination of SDF-1, CX-CR4, and VEGF levels

[0035] 100 μL of serum under item 2.2.1 was added to the multifunctional enzyme marker micro-well, incubated at 37°C for 2 h, 100 μL of detection antibody diluent was added to each well, the micro-well plate was sealed with adhesive tape and incubated at 37°C for 1 h, the micro-well was rinsed, 100 μL of enzyme-labeled antibody was added to each well, the micro-well plate was sealed with adhesive tape and incubated at 37°C for 30 min, and the rinsing operation was repeated. 100 μL of substrate solution containing SDF-1, CX-CR4, and VEGF was added and placed at 37°C for 10 min, 100 μL of H2SO4 termination solution was added to each well to terminate the reaction, and the OD value was detected at 450 nm, 465 nm, and 492 nm.

[0036] 2.2.3 Data processing method

[0037] The experimental data were processed by SPSS 22.0 software, the data were represented by ( ), one-way ANOVA was used, and t-test was used. P<0.05 was considered statistically significant.

[0038] 3 Experimental results

[0039] 3.1 Effect of Guqiaohuoxue Capsules on serum TC, TG, and LDL-C levels in rats with carotid artery sclerosis

[0040] The results of serum TC, TG, and LDL-C detection in each group of rats are shown in Table 1. Compared with the blank control group, the TG, TC, and LDL-C levels in the model control group were significantly increased (P<0.01, P<0.001), and the TC, TG, and LDL-C levels in the positive control group and Guqiaohuoxue Capsules group were significantly lower than those in the model control group (P<0.05, P<0.01, P<0.001).

[0041] Table 1 Comparison of TC, TG, and LDL-C detection results in each group of rats

[0042]

[0043] Note: Compared with the blank control group, “ ## ” indicates P<0.01, “ ### ” indicates P<0.001, compared with the model control group, “ * ” indicates P<0.05, and “ **" indicates P < 0.01, " *** " indicates that P < 0.001.

[0044] 3.2 Effects of Guiqi Huoxue Capsules on Serum SDF-1, CX-CR4, and VEGF Levels in Rats with Carotid Artery Atherosclerosis

[0045] The levels of SDF-1, CX-CR4, and VEGF in each group of rats are shown in Table 2. Compared with the blank control group, the levels of SDF-1, CX-CR4, and VEGF in the model control group were significantly increased (P < 0.001), while the levels of SDF-1, CX-CR4, and VEGF in the positive control group and the Guiqi Huoxue Capsule group were significantly decreased compared with the model control group (P < 0.01, P < 0.001).

[0046] Table 2 Comparison of SDF-1, CX-CR4, and VEGF levels in rats of different groups

[0047]

[0048] Note: Compared with the blank control group, " ### "" indicates P < 0.001, compared with the model control group, ** " indicates P < 0.01, " *** " indicates that P < 0.001.

[0049] SDF-1 (serial stromal cell-derived factor-1) is a chemokine produced by bone marrow cells that significantly induces the migration of monocytes, smooth muscle cells, lymphocytes, and leukocytes. CX-CR4 (chemokine receptor-4) is the receptor for SDF-1. After binding to SDF-1, it forms a homodimer, stimulating smooth muscle cell proliferation and migration into the subendothelial region, thereby damaging endothelial cells, exposing collagen tissue, inducing platelet aggregation and activation, and exacerbating atherosclerosis. VEGF (vascular endothelial growth factor) promotes extracellular matrix degeneration, vascular endothelial cell migration and proliferation, and is closely related to arteriosclerosis.

[0050] This study shows that Guiqi Huoxue Capsules can reduce serum TC, TG, and LDL-C in rats with carotid artery sclerosis, and can significantly inhibit the levels of SDF-1, CX-CR4, and VEGF in rats, thereby reducing the degree of carotid artery sclerosis plaques and alleviating the symptoms of arteriosclerosis.

[0051] Experimental Example 2: Effects of Guiqi Huoxue Capsules on a Rat Model of Cerebral Arteriosclerosis

[0052] 1. Experimental Materials

[0053] 1.1 Laboratory Animals

[0054] Healthy clean adult male Wistar rats 60, body weight 200±20g, provided by LuNan Pharmaceutical Group Co., Ltd., license: SYXK(Lu)2018-0008, fed in LuNan Pharmaceutical Group pharmacological center, all rats were adaptively cultured for 1 week with ordinary feed.

[0055] 1.2 Reagents, drugs and instruments

[0056] TRIzol reagent, Invitrogen Corporation, USA; total cholesterol (TC), triglyceride (TG) and low density lipoprotein cholesterol (LDL-C) assay kit, endothelin (ET) kit, nitric oxide (NO) kit, thromboxane B2 (TXB2) kit, 6-keto-prostaglandin F1a (6-keto-PGF1a) kit, all purchased from Nanjing Jiancheng Biological Engineering Institute. Guili Xian Capsules, GMP: Z20090686, LuNan Hupu Pharmaceutical Co., Ltd. produced. Cinnarizine tablets, GMP: H11021285, Beijing Wan Hui Shuanghe Pharmaceutical Co., Ltd. Automatic biochemical analyzer, Japan Toshiba Corporation.

[0057] 2 Experimental method

[0058] 2.1 Animal grouping, modeling and administration

[0059] From 60 rats, 50 rats were randomly selected to be fasted for 12h, and after intraperitoneal injection of 10% chloral hydrate, bilateral renal aortic stenosis operation was performed to make it 3 / 4 stenosis, to cause experimental hypertension model of rats. After 1 week of operation, the model rats were given high-fat feed (containing 81.3% basic feed, 3% cholesterol, 0.5% sodium cholate, 0.2% propylthiouracil, 5% sugar, 10% lard) once a day, for a total of 14 weeks, to make a cerebral arteriosclerosis model of hypertension and hyperlipidemia. Another 10 rats were only subjected to bilateral renal artery dissection without stenosis, and were given ordinary feed for 14 consecutive weeks.

[0060] The 50 model rats were randomly divided into 5 groups, 10 rats in each group, namely model control group, positive control group, test low, medium and high dose groups. The positive control group was given cinnarizine tablets 6.75mg / kg by gavage from 6 weeks after operation, for 8 consecutive weeks. The test low, medium and high dose groups were given Guili Xian Capsules 0.22g / kg, 0.43g / kg, 0.86g / kg by gavage from 6 weeks after operation, for 8 consecutive weeks. The blank control group and the model control group were given the same amount of sterile drinking water.

[0061] 2.2 Index determination

[0062] 2.2.1 Blood pressure determination of rats in each group

[0063] Fifteen weeks after the operation, the rats in each group were fasted for 12 hours, weighed, and anesthetized by intraperitoneal injection of 10% water and chloral. The left common carotid artery was isolated, cannulated, and stabilized for 30 minutes. Systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) were recorded using a TSD-104A pressure transducer.

[0064] 2.2.2 Detection of TC, TG, and LDL-C

[0065] 2.2.2 After the blood pressure test, 5 mL of blood was drawn from the abdominal aorta, centrifuged, and serum was collected. The levels of TC, TG, and LGL-C were measured using a fully automated biochemical analyzer via chemical enzymatic method.

[0066] 2.2.3 Plasma ET, NO, TXB2, 6-keto-PGF 1α Content determination

[0067] Blood was collected from the abdominal aorta of rats in each group (3 mL). The blood was added to test tubes containing 2% EDTA disodium and aprotinin, mixed thoroughly, and the plasma was separated by centrifugation. NO was measured using the nitrate reductase method, and ET, TXB2, and 6-keto-PGF were measured using radioimmunoassay. 1α .

[0068] 2.2.4 Data Processing Methods

[0069] Experimental data were processed using SPSS 22.0 software, and the data are presented in (…). The results were analyzed using one-way ANOVA and t-tests. A p-value < 0.05 was considered statistically significant.

[0070] 3 Experimental Results

[0071] 3.1 Effects of Guiqi Huoxue Capsules on Blood Pressure in Rats with Hypertension and Cerebral Arteriosclerosis

[0072] The blood pressure of rats in each group is shown in Table 3. Compared with the blank control group, the SBP, DBP, and MAP of rats in the model control group were significantly increased (P<0.01, P<0.001). Compared with the model control group, the SBP, DBP, and MAP of rats in each treatment group were significantly decreased. There were significant differences between the positive control group and the medium and high dose groups in the experiment (P<0.05, P<0.01, P<0.001).

[0073] Table 3 Comparison of SBP, DBP, and MAP results in rats of different groups

[0074]

[0075] Note: Compared with the blank control group, " ### "" indicates P < 0.001, compared with the model control group, *" means P<0.05, ** " means P<0.01, *** " means P<0.001.

[0076] 3.2 Effect of Guiqi Huoxue Capsule on serum TC, TG and LDL-C of rats with hypertension and cerebral arteriosclerosis

[0077] The results of serum TC, TG and LDL-C of rats in each group were shown in Table 4. Compared with the blank control group, the levels of TG, TC and LDL-C of rats in the model control group were significantly increased (P<0.001). Compared with the model control group, the levels of TC, TG and LDL-C of rats in the positive control group and the high and middle dose groups of the test were significantly decreased (P<0.01, P<0.001).

[0078] Table 4 Comparison of the results of TC, TG and LDL-C of rats in each group

[0079]

[0080] Note: Compared with the blank control group, ### " means P<0.001, compared with the model control group, ** " means P<0.01, *** " means P<0.001.

[0081] 3.3 Effect of Guiqi Huoxue Capsule on plasma ET and NO levels of rats with hypertension and cerebral arteriosclerosis

[0082] Modern medicine believes that ET is a very strong long-acting vasoconstrictor, which can cause vasoconstriction, platelet aggregation and smooth muscle cell proliferation, and is a significant feature of damaged arterial endothelium, and has a definite relationship with the development of arteriosclerosis. NO is an endothelium-derived vasodilator in the body, which can increase cerebral blood flow, resist platelet and leukocyte aggregation adhesion, enhance synaptic transmission, and inhibit the production of endothelin.

[0083] The results of ET and NO levels of rats in each group were shown in Table 5. Compared with the blank control group, the ET content of rats in the model control group was significantly increased (P<0.001). Compared with the model control group, the ET content of rats in each treatment group was decreased, and the ET content of rats in the positive drug control group and the high dose group of the test was close to that of the blank control group. Compared with the blank control group, the NO content of rats in the model control group was significantly decreased (P<0.05). Compared with the model control group, the NO content of rats in the positive control group and the high dose group of the test was significantly increased, with significant difference (P<0.05).

[0084] Table 5 Comparison of the results of ET and NO levels of rats in each group

[0085]

[0086]

[0087] Note: Compared with the blank control group, # P<0.05, and ### P<0.001; compared with the model control group, * P<0.05, and ** P<0.01, and *** P<0.001.

[0088] 3.4 Effects of Guizhi Huoxue Capsule on TXB2 and 6-keto-PGF 1α levels in rats with hypertension and cerebral arteriosclerosis

[0089] TXB2 is a metabolite of thromboxane A2, which has strong vasoconstriction, promotes platelet aggregation, and leads to thrombosis. Therefore, tracking the content of TXB2 can directly reflect the blood stasis in vivo. 6-keto-PGF 1α is a metabolite of PGI2, which is produced by vascular endothelium and has strong vasodilating and platelet aggregation inhibiting effects. A decrease in 6-keto-PGF 1α level indicates that blood stasis is aggravated.

[0090] The results of TXB2 and 6-keto-PGF 1α levels in rats in each group are shown in Table 6. Compared with the blank control group, the TXB2 and 6-keto-PGF 1α levels in rats in the model control group were significantly decreased (P<0.001). Compared with the model control group, the TXB2 level in rats in the positive control group and the test high-dose group was significantly increased (P<0.01, P<0.001), and the 6-keto-PGF 1α level in rats in the positive control group and the test high-dose group was significantly increased (P<0.05, P<0.01).

[0091] Table 6 Comparison of TXB2 and 6-keto-PGF 1α levels in rats in each group

[0092]

[0093] Note: Compared with the blank control group, ### P<0.001; compared with the model control group, * P<0.05, and **" indicates P<0.01, *** " indicates P<0.001.

[0094] The above study shows that Guqiaohuo capsule can reduce blood viscosity, dilate blood vessels, improve blood flow, significantly improve lipid metabolism disorder, regulate NO, ET, TXB2, 6-keto-PGF 1α level, and further regulate vascular function, significantly reduce the risk of cerebral arteriosclerosis, inhibit the progression of cerebral arteriosclerosis, and relieve the symptoms of cerebral arteriosclerosis. Guqiaohuo capsule has a positive therapeutic effect on arteriosclerosis, especially cerebral arteriosclerosis.

Claims

1. The use of Guiqi Huoxue Capsules in the preparation of a medicament for treating arteriosclerosis; the arteriosclerosis is cerebral arteriosclerosis or carotid arteriosclerosis.

2. Use according to claim 1, characterized in that, The cerebral arteriosclerosis or carotid arteriosclerosis is of the type of qi deficiency and blood stasis, the type of deficiency of both qi and blood, the type of phlegm turbidity obstruction or the type of phlegm and blood stasis mutual obstruction.

3. Use according to claim 2, characterized in that, The cerebral arteriosclerosis or carotid arteriosclerosis is of the type of qi deficiency and blood stasis.

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