Preparation method and application of medicinal and edible traditional Chinese medicine compound with effect of treating uric acid diseases

Abstract

The invention discloses a preparation method and application of a medicinal and edible traditional Chinese medicine compound with an effect of treating uric acid diseases. The traditional Chinese medicine composition is prepared from the following raw materials in parts by weight: 15 to 25 parts of semen plantaginis, 15 to 25 parts of pawpaw, 5 to 15 parts of rhizoma smilacis glabrae, 5 to 15 parts of herba portulacae, 1 to 11 parts of radix glycyrrhizae preparata, 5 to 15 parts of folium mori, 5 to 15 parts of folium perillae, 1 to 11 parts of semen pruni, 5 to 15 parts of rhizoma polygonati, 1 to 11 parts of black dates and 1 to 9 parts of mulberries. The traditional Chinese medicine compound is composed of medicinal and edible raw materials, has stable efficacy of reducing uric acid and relieving uric acid liver and kidney injury, renal fibrosis and gouty arthritis, can relieve arthrocele caused by gout, reduces the level of joint inflammatory factors and the like, and takes effect quickly. The traditional Chinese medicine composition can be used for treating hyperuricemia, uric acid nephropathy, gouty arthritis and hyperuricemia accompanying symptoms.

Description

Technical Field

[0001] This invention relates to the field of traditional Chinese medicine, specifically to a method for preparing and applying a compound of medicinal and edible herbs that has the effect of treating uric acid diseases. Background Technology

[0002] Hyperuricemia is a systemic metabolic disease caused by a disorder in the biosynthesis and metabolism of purines in the body, leading to excessive uric acid production and / or impaired renal excretion, resulting in a persistently elevated serum urate concentration exceeding the physiological normal range. According to current clinical guidelines, a fasting serum uric acid level higher than 420 μmol / L (7 mg / dL) on two separate occasions is generally considered the diagnostic criterion for hyperuricemia. This state forms the biochemical basis for a series of subsequent pathological changes. Its core danger lies in the fact that when the serum uric acid concentration exceeds its solubility in body fluids, it precipitates as monosodium urate crystals in tissues and organs. This process is often asymptomatic in its early stages, but it continuously and insidiously damages the function of organs and tissues. This process occurs because approximately two-thirds of uric acid is excreted by the kidneys, and the complex reabsorption mechanism of the renal tubules means that only a small amount of uric acid is ultimately excreted.

[0003] A high uric acid environment can damage body tissues, particularly the liver and kidneys, which are responsible for uric acid formation. The liver is a vital organ for metabolizing uric acid; excessively high uric acid concentrations can damage liver cells. Uric acid accumulation in the liver can lead to fat buildup, resulting in fatty liver disease, and even hepatitis or cirrhosis. The kidneys are responsible for excreting uric acid; high uric acid levels increase the burden on the kidneys, and this overload can weaken kidney function. Uric acid crystals can deposit in the kidneys, forming uric acid kidney stones, which can cause renal colic and hematuria, eventually leading to chronic kidney disease and even kidney failure. Furthermore, hyperuricemia may be associated with metabolic diseases such as hypertension and diabetes, which can also damage the kidneys, creating a vicious cycle.

[0004] Furthermore, the deposition of monosodium urate crystals in the joint cavity and surrounding soft tissues is a direct trigger for gouty arthritis. These tiny crystals can activate the body's inherent immune response, recruiting a large number of inflammatory cells, such as neutrophils, to the deposition site, releasing various pro-inflammatory factors, thus triggering a severe, usually self-limiting, acute inflammatory response. Clinically, this manifests as redness, swelling, heat, pain, and dysfunction of the joints, most commonly the first metatarsophalangeal joint. If hyperuricemia is not effectively controlled for a long period, repeated attacks of acute arthritis will gradually evolve into chronic, destructive tophaceous arthritis, leading to persistent joint pain, stiffness, and even deformity, severely impacting the patient's quality of life.

[0005] Currently, first-line chemotherapy drugs, such as allopurinol and febuxostat which inhibit uric acid synthesis, or benzbromarone which promotes uric acid excretion, can effectively lower serum uric acid levels. However, their use is often accompanied by significant limitations, including potential serious hypersensitivity reactions, cardiovascular safety risks, and adverse events such as hepatotoxicity and nephrotoxicity. This makes it difficult for many patients to adhere to long-term treatment and limits their universality in prevention and long-term management. Furthermore, most drugs cannot simultaneously treat the complications of hyperuricemia, and the damaging effects of these drugs exacerbate the dual harm to the body from both the disease and the medication, thereby inducing the development of chronic diseases and increasing the difficulty and duration of treatment.

[0006] Given the safety concerns associated with the long-term use of chemical drugs, academia and industry are actively seeking safer, gentler, and more suitable intervention methods for long-term use from traditional Chinese medicine resources. Substances derived from both food and medicine have thus demonstrated enormous application potential. These substances, derived from natural foods, possess both nutritional supplementation and physiological regulation functions. Their high safety and minimal side effects align perfectly with the health philosophy of "prevention first, long-term management" for chronic metabolic diseases such as hyperuricemia. Therefore, based on the theory of "food and medicine sharing the same origin," using modern science and technology to screen and develop compound functional foods that can effectively and safely intervene in hyperuricemia, gout, and chronic kidney disease has become an important research direction in this field. Food and medicine homology drugs have a milder damaging effect on the body, while also possessing nourishing effects, and have good therapeutic and preventative effects on diseases and their comorbidities.

[0007] Currently, Chinese invention patent CN109364199A discloses a formula for treating gout, characterized by comprising the following raw materials in parts by weight: 6-18 parts of kudzu root, 8-16 parts of rhubarb, 4-13 parts of dioscorea hypoglauca, 2-7 parts of lysimachia christinae, 2-6 parts of Liquidambar formosana, 12-18 parts of coix seed, 8-20 parts of honeysuckle vine, 9-17 parts of rehmannia root, 10-15 parts of smilax glabra, 4-9 parts of lily bulb, 15-22 parts of plantain seed, 5-12 parts of mulberry twig, 10-15 parts of drynaria rhizome, 3-7 parts of earthworm, 5-20 parts of clematis root, 15-23 parts of notoginseng, 18-27 parts of polygonum cuspidatum, and 5-11 parts of licorice root. However, the drawback of this formula is that its complex composition, which includes as many as eighteen medicinal herbs, not only increases the economic burden on patients due to its high cost and difficulty in quality control, but also poses a potential safety hazard of long-term use on liver and kidney function.

[0008] Currently, Chinese invention patent CN114848746B discloses a traditional Chinese medicine compound for treating hyperuricemia and gouty arthritis. The components, by weight, are: Astragalus membranaceus 5-15 parts, Lilium brownii 5-15 parts, Plantago asiatica 5-15 parts, Glycyrrhiza uralensis 5-15 parts, Lysimachia christinae 10-20 parts, Dipsacus asper 5-15 parts, Clematis chinensis 5-15 parts, and Rheum palmatum 1-10 parts. The main drawback of this compound is that it contains Rheum palmatum and Clematis chinensis, which are explicitly not listed in the catalogue of medicinal and edible herbs. This fundamentally limits the product's properties and application scope, making it unsuitable for development as a health food or ordinary food, and unsuitable as a daily supplement for long-term use by the general population, thus weakening its value in "prevention." Furthermore, the compound disclosed in this invention is more effective, has a more significant effect, and a wider treatment range than the compound disclosed in CN114848746B.

[0009] In summary, existing technologies for using food-medicine homologous substances to intervene in hyperuricemia, gout, and chronic kidney disease and other complications of hyperuricemia still have a series of problems, such as complex formulations, high costs, the presence of non-food-medicine homologous ingredients which limits their application, or unclear synergistic effects and unstable efficacy even though they are food-medicine homologous substances. Summary of the Invention

[0010] The purpose of this invention is to overcome the shortcomings of the prior art and to provide a preparation method and application of a traditional Chinese medicine compound with therapeutic effects on uric acid diseases. The compound formulation of this invention is more concise, cost-controllable, and the materials are entirely based on the list of traditional Chinese medicines with the same origin. Moreover, the components can play a significant synergistic role in reducing serum uric acid, inhibiting gouty arthritis, and alleviating uric acid-induced liver and kidney damage and renal fibrosis. It has important practical significance and application value for meeting the health needs of the vast population with hyperuricemia, gout and chronic kidney disease.

[0011] To achieve the above objectives, the technical solution designed by the present invention is as follows: This invention provides a medicinal and edible herbal compound for treating uric acid diseases. The raw materials of the herbal compound, by weight, include 15-25 parts of Plantago asiatica, 15-25 parts of Chaenomeles speciosa, 5-15 parts of Smilax glabra, 5-15 parts of Portulaca oleracea, 1-11 parts of Glycyrrhiza uralensis (processed), 5-15 parts of Morus alba leaves, 5-15 parts of Perilla frutescens leaves, 1-11 parts of Prunus japonica seeds, 5-15 parts of Polygonatum sibiricum, 1-11 parts of Ziziphus jujuba, and 1-9 parts of Morus alba fruit.

[0012] Furthermore, the raw materials of the traditional Chinese medicine compound, by weight, include 17-23 parts of Plantago asiatica, 17-23 parts of Chaenomeles speciosa, 7-13 parts of Smilax glabra, 7-13 parts of Portulaca oleracea, 3-9 parts of Glycyrrhiza uralensis (processed), 7-13 parts of Morus alba leaves, 7-13 parts of Perilla frutescens leaves, 3-9 parts of Prunus japonica seeds, 7-13 parts of Polygonatum sibiricum, 3-9 parts of Ziziphus jujuba, and 1-7 parts of Morus alba fruit.

[0013] Furthermore, the raw materials of the Chinese herbal compound, by weight, include 20 parts of plantain seed, 20 parts of papaya, 10 parts of smilax glabra, 6 parts of prepared licorice root, 10 parts of mulberry leaf, 10 parts of perilla leaf, 6 parts of apricot kernel, 10 parts of polygonatum rhizome, 6 parts of black dates, and 4 parts of mulberry fruit.

[0014] This invention also provides a method for preparing the above-mentioned medicinal and edible herbal compound with therapeutic effects on uric acid diseases, comprising the following steps: 1) Weigh out the following ingredients according to the above weight ratio: plantain seed, papaya, smilax glabra, purslane, prepared licorice root, mulberry leaf, perilla leaf, apricot kernel, polygonatum rhizome, black date, and mulberry. Soak them in water, heat over high heat until boiling, then reduce to low heat and pour out the first decoction. Add water again and heat to obtain the second decoction. 2) Mix the two solutions to obtain a traditional Chinese medicine compound.

[0015] The present invention also provides the application of the above-mentioned medicinal and edible herbal compound with therapeutic effects on uric acid diseases in the preparation of traditional Chinese medicine preparations.

[0016] The present invention also provides a traditional Chinese medicine preparation, which includes the above-mentioned traditional Chinese medicine compound and pharmaceutically acceptable excipients (for personalized taste improvement).

[0017] Furthermore, the excipients are any one or more of vitamin C, sorbitol, mannitol, xylitol, fructose, amino acids, meglumine, dextrin, magnesium stearate, sucrose, and citric acid.

[0018] Furthermore, the traditional Chinese medicine preparation is any one of the following: powder, oral liquid, granules, tablets, capsules, pills, syrups, and ointments.

[0019] The pharmacological properties of this invention are as follows: The traditional Chinese medicine compound of this invention has the main effects of promoting diuresis and eliminating dampness, relieving numbness and swelling, and tonifying qi and strengthening the exterior. Plantain seed, Smilax glabra, Chaenomeles speciosa, and Portulaca oleracea are the principal herbs, which have the effects of promoting diuresis and eliminating dampness, relieving numbness and swelling; Polygonatum sibiricum, black dates, mulberry leaves, and Perilla frutescens are the assistant herbs. The former two play the role of tonifying qi and nourishing yin, strengthening the defensive qi and strengthening the exterior, and invigorating the spleen and moistening the lungs, while the latter two play the role of... Regulate Qi and resolve phlegm It has anti-inflammatory and swelling-reducing effects; Prunus japonica seed is used as an adjuvant, which has the effect of moistening the intestines and promoting bowel movements. Lowering Qi and promoting urination The medicinal effects are as follows: Prepared licorice root and mulberry are used as guiding herbs to invigorate qi, nourish yin, and replenish blood. All the herbs mentioned are harmonized.

[0020] The beneficial effects of this invention are: The traditional Chinese medicine compound of this invention has stable effects in lowering uric acid and relieving uric acid-induced liver and kidney damage, renal fibrosis, and gouty arthritis. It can reduce joint swelling caused by gout, lower the level of inflammatory factors in the joints, and has a rapid onset of action. It can be used to treat hyperuricemia, uric acid-induced liver and kidney damage, gouty arthritis, and chronic kidney disease.

[0021] 2. The medicinal materials used in the traditional Chinese medicine compound formula of this invention are low-cost and readily available. All the raw materials used in this formula are food-grade medicinal materials, ensuring high safety and applicability with no significant side effects. The treatment course is short; patients with hyperuricemia, uric acid-induced liver and kidney damage, gouty arthritis, and chronic kidney disease can show good efficacy after 7-14 days of treatment, with stable efficacy. The formula can be prepared as a decoction, which is simple to prepare and suitable for daily use. The powder prepared from this formula is fast-acting and easily absorbed. The granules prepared from this formula are easy to store, palatable, and convenient to take. Attached Figure Description

[0022] Figure 1 Figure showing the effect of a traditional Chinese medicine compound with therapeutic effects on uric acid diseases on the renal serum biochemistry of mice with high uric acid. Where A represents the mouse serum UA level graph. B is a graph showing the UREA level in mouse serum. C represents the mouse serum CREA level graph. Figure 2 Figure showing the effect of a traditional Chinese medicine compound with therapeutic effects on uric acid diseases on kidney tissue sections of mice with high uric acid. Figure 3 The effect of a traditional Chinese medicine compound with therapeutic effects on uric acid diseases on liver serum biochemistry in mice with high uric acid levels is shown in the figure. In this figure, A represents the serum ALP level in mice. B is a graph showing the serum γ-GT levels in mice. C represents the serum ALT level in mice. D is a graph showing mouse serum AST levels. Figure 4 The effect of a traditional Chinese medicine compound derived from food and medicine on liver XOD in mice with hyperuricemia on liver and kidney damage, gouty arthritis and chronic kidney disease. Figure 5 The effect of a traditional Chinese medicine compound with medicinal and edible properties on liver tissue sections of mice with hyperuricemia on liver and kidney damage, gouty arthritis and chronic kidney disease caused by hyperuricemia; Figure 6 Figure showing the effect of a traditional Chinese medicine compound with therapeutic effects on uric acid diseases on the HK-2 cell fibrosis model; In this diagram, A represents the VIM gene expression level in HK-2 cells. B is a graph showing the FN1 gene expression level in HK-2 cells. C represents the COL1A1 gene expression level in HK-2 cells. D represents the COL3A1 gene expression level in HK-2 cells. E represents the TGF-β2 gene expression level in HK-2 cells. Figure 7 Figure showing the effect of a traditional Chinese medicine compound with therapeutic effects on uric acid diseases on ankle swelling in rats with hyperuricemia. In this figure, A represents the swelling changes (compared to the post-modeling state). B shows the swelling changes (compared to before modeling). C shows the changes in swelling during the experiment. Figure 8 Figure showing the effect of a traditional Chinese medicine compound with therapeutic effects on uric acid diseases on inflammatory factors in the ankle joint of rats with hyperuricemia. Figure 9 This figure shows the effect of a traditional Chinese medicine compound with therapeutic effects on uric acid diseases on a tissue section of the ankle joint of a rat with hyperuricemia. Detailed Implementation

[0023] The present invention will now be described in further detail with reference to specific embodiments, so that those skilled in the art can understand it.

[0024] Example 1 The raw materials of the medicinal and edible compound formula 1, which has the effect of treating uric acid diseases, are: 20 g of plantain seed, 20 g of papaya, 10 g of smilax glabra, 10 g of purslane, 6 g of prepared licorice root, 10 g of mulberry leaf, 10 g of perilla leaf, 6 g of apricot kernel, 10 g of polygonatum rhizome, 6 g of black date, and 4 g of mulberry.

[0025] All the Chinese medicinal materials mentioned above were purchased from Hubei Zhihetang Pharmacy Co., Ltd., and were accurately weighed before being used in subsequent experiments.

[0026] The preparation method of the above-mentioned traditional Chinese medicine compound 1 includes the following steps: 1) Weigh out 20 g of Plantago seed, 20 g of papaya, 10 g of Smilax glabra, 10 g of Portulaca oleracea, 6 g of prepared licorice root, 10 g of mulberry leaf, 10 g of Perilla leaf, 6 g of Prunus japonica seed, 10 g of Polygonatum sibiricum, 6 g of black dates, and 4 g of mulberry fruit. Soak in cold water (distilled water) for 20 minutes, with the water level 2-3 cm above the herbs (or according to a material-to-liquid ratio of 1:6, w / v). Heat over high heat until boiling, then simmer over low heat for 25 minutes (starting from the boiling point). Pour out the first decoction, add an appropriate amount of warm water, and heat for another 15 minutes to obtain the second decoction.

[0027] 2) The two mixtures of the medicinal liquids yielded the traditional Chinese medicine compound formula 1.

[0028] Example 2 The traditional Chinese medicine compound 2 prepared in this embodiment is basically the same as that in Example 1, except that: The raw materials of the above-mentioned Chinese herbal compound 2, by weight, include 25 g of plantain seed, 25 g of papaya, 15 g of smilax glabra, 15 g of purslane, 11 g of prepared licorice root, 15 g of mulberry leaf, 15 g of perilla leaf, 11 g of apricot kernel, 15 g of polygonatum rhizome, 11 g of black dates, and 9 g of mulberry.

[0029] Example 3 The traditional Chinese medicine compound 2 prepared in this embodiment is basically the same as that in Example 1, except that: The raw materials of the above-mentioned Chinese herbal compound 2, by weight, include 15 g of plantain seed, 15 g of papaya, 5 g of smilax glabra, 5 g of purslane, 1 g of prepared licorice root, 5 g of mulberry leaf, 5 g of perilla leaf, 1 g of apricot kernel, 5 g of polygonatum rhizome, 1 g of black date, and 0.7 g of mulberry.

[0030] Examples 4-6: Traditional Chinese Medicine Preparations The Chinese herbal compound decoctions 1-3 correspond to the above-mentioned Chinese herbal compound formulas 1-3 respectively.

[0031] In the embodiments, the direct Chinese medicine compound 1-3 is used as the Chinese medicine compound decoction 1-3. According to the actual situation, different excipients are added to improve the taste during the preparation of the Chinese medicine compound decoction 1-3; among them, the excipients are citric acid and / or sucrose.

[0032] The efficacy of the traditional Chinese medicine compound decoction prepared according to Example 4 was verified as follows: 1. Verify the effectiveness of compound traditional Chinese medicine decoction 1 (1) Experimental materials 1.1 Drugs: The traditional Chinese medicine compound decoction 1 was filtered through sterile gauze and concentrated to a relative crude drug concentration of 1 g / mL; as well as physiological saline, allopurinol (AP), adenine, potassium oxonate, yeast extract and sodium carboxymethyl cellulose (CMC-Na).

[0033] 1.2 Animals: a. [Mice] Male Kunming mice (SPF grade), weighing 35±2g, were purchased from the Animal Center of Huazhong Agricultural University. All mice were housed in an SPF animal room with suitable temperature and humidity. Six mice per cage were provided with normal food and water during the experiment.

[0034] b. [Rats] Male SD rats (SPF grade), weighing 180±20g, were purchased from the Animal Center of Huazhong Agricultural University. All rats were housed in an SPF animal room with suitable temperature and humidity. Three rats per cage were provided with normal food and water during the experiment.

[0035] 1.3 Reagent Kits: Biochemical assay kits, such as the xanthine oxidase (XOD) assay kit, were purchased from Nanjing Jiancheng Bioengineering Institute. BCA protein concentration kits were purchased from Beyotime Biotechnology Co., Ltd. All reagent kits were used in accordance with the instructions provided within the kit.

[0036] (2) Experimental methods 2.1 Animal grouping and treatment a. [Mice] Thirty-six healthy SPF-grade Kunming mice were randomly divided into four groups of nine mice each: a blank control group, a model group, an experimental group, and a positive control group. A hyperuricemia model was established. Except for the blank control group, all groups were administered adenine (200 mg / kg / d) + potassium oxonate (250 mg / kg / d) + yeast extract (300 mg / kg / d) by gavage. The blank control group was administered an equal amount of CMC-Na (0.5%) by gavage. One hour later, all groups received the corresponding drug intervention (the blank control group and model group were administered an equal amount of CMC-Na orally, the experimental group received 18.9 g / kg of traditional Chinese medicine compound 1), and the positive control group received AP (20 mg / kg / d). All groups were administered this method continuously for 7 days. Blood was collected on days 1, 4, and 7, including ocular blood collection. Mice were euthanized by cervical dislocation and samples were collected.

[0037] b. [Rat] Eighteen healthy SPF-grade SD rats were randomly divided into three groups of six each: a blank control group, a model group, and an experimental group. Before the experiment, a circular mark was made on the right ankle joint of each rat with a black oil-based pen, and this circular line was used as the marker.

[0038] Rats in the model group and experimental group were administered potassium oxonate (1.5 g / kg) once daily by gavage, while the blank control group was administered an equal volume of CMC-Na (0.5%) by gavage for 12 consecutive days. On day 5, rats were anesthetized by intraperitoneal injection of 10% chloral hydrate at 3 mL / kg. Except for the blank control group, all rats were injected with 0.4 mL of sodium urate solution (50 mg / mL) into the joint cavity by inserting a disposable sterile syringe at 30°–45° posterior to the Achilles tendon. Successful injection resulted in bulging of the joint capsule on the opposite side. Except for the blank control group, all rats exhibited lameness and ataxia when walking.

[0039] One hour after modeling, the rats in the experimental group were administered 9.45 g / kg of the traditional Chinese medicine compound decoction 1, while the blank control group and the experimental group were administered the same amount of sodium carboxymethyl cellulose by gavage for 7 consecutive days. On the last day, the rats were anesthetized, euthanized, and then samples were collected.

[0040] c. [HK-2 cells] The model group and experimental group were induced with TGF-β (10μM) for 24h to construct a renal cell fibrosis model. The experimental group was treated with MEM medium containing 4.78 mg / mL of lyophilized Chinese medicine compound 1 for 24h, while the blank control group and experimental group were treated with MEM medium for 24h.

[0041] 2.2 Detection Measurement of renal markers (UA, CREA, UREA) and hepatic markers (ALP, γ-GT, ALT, AST) in mouse serum: Anticoagulated blood from mice was collected and centrifuged at 5000 rpm for 10 minutes to separate the serum. Serum biochemical indicators were detected using a biochemical analyzer.

[0042] Xanthine oxidase (XOD) assay in mouse liver: Collected mouse liver tissue was homogenized with physiological saline, and protein concentration was detected using a BCA kit. XOD activity in mouse liver was measured according to the kit's instructions.

[0043] Mouse liver and kidney tissue sections: Liver and kidney tissues were collected, fixed with 4% paraformaldehyde, prepared into paraffin sections, and stained with H&E.

[0044] Fibrosis gene expression in HK-2 cells: RNA was extracted from HK-2 cells after the experiment, and the mRNA levels of TGF-β2, Collagen I (COL1A1), Collagen III (COL3A1), Fibronectin (FN), and Vimentin (VIM) were detected by RT-qPCR.

[0045] Ankle joint of rats: The width of the ankle joint was recorded daily after day 5 of the experiment. The joint and toes below the marked line were completely immersed in the measuring device to obtain the ankle joint width at that time.

[0046] Inflammatory factors: Tissue samples were collected from around the ankle joint of rats, and the protein levels of IL-6, IL-1β, and TNF-α in the tissues were detected using Western blot.

[0047] Rat ankle joint sections: tissues around the rat ankle joint were collected, fixed with 4% paraformaldehyde, decalcified, and then prepared into paraffin sections for H&E staining.

[0048] (3) Experimental results 3.1 Biochemistry of mouse kidney serum Experimental results show that ( Figure 1The UA levels in the model group mice were significantly upregulated during the experiment. UA is a core indicator for detecting hyperuricemia. The upregulation of serum UA verified the successful construction of the mouse hyperuricemia model. After treatment with the traditional Chinese medicine compound in this example, the UA levels in the mice were significantly lower than those in the model group, indicating that the traditional Chinese medicine compound in this example has a good uric acid-lowering effect, and the effect was significant from day 1 to day 7 of administration.

[0049] In addition, CREA in the model group mice did not change significantly during the experiment, while UREA was significantly upregulated on day 4 and remained different from the blank control group after day 7. UREA is the end product of protein metabolism, and the upregulation of UREA in serum indicates that the mice's kidneys were damaged. After treatment with the traditional Chinese medicine compound in this example, the mice's UREA level returned to normal, suggesting that the traditional Chinese medicine compound in this example can repair kidney damage in mice with hyperuricemia.

[0050] 3.2 Mouse kidney tissue sections Experimental results show that ( Figure 2 In the blank control group, the kidney tissue structure and morphology were normal, with clear renal tubular and glomerular structures and tightly and orderly arranged renal tubular epithelial cells. In the model group, glomerular atrophy (marked with an asterisk) and inflammatory cell infiltration (marked with an arrow) were observed in the renal interstitium. Compared with the model group, the positive control group still showed renal tubular dilation and glomerular atrophy, while the damage to glomeruli and tubules was improved in the experimental group. This suggests that the traditional Chinese medicine compound in this example can alleviate kidney damage caused by hyperuricemia.

[0051] 3.3 Biochemistry of mouse liver serum ALB, γGT, ALT, and AST are important indicators for monitoring liver health. Experimental results show that ( Figure 3 Compared with the blank control group, the serum biochemical levels in the model group increased significantly after day 4, indicating that the hyperuricemia model not only damages kidney function but also liver function. The experimental group significantly downregulated the levels of γGT and AST in serum. After day 7, the levels of the four indicators in the experimental group were significantly lower than those in the model group. The positive control group suggests that the traditional Chinese medicine compound in this example can alleviate liver damage caused by hyperuricemia.

[0052] 3.4 XOD activity in mouse liver Experimental results show that ( Figure 4In the model group mice, XOD levels were significantly upregulated. XOD is mainly found in the milk, liver, and spleen of mammals and is an important enzyme in nucleic acid metabolism. This enzyme level increases significantly when the liver is damaged. The upregulation of XOD in the liver reflects the successful establishment of the mouse hyperuricemia model. After treatment with the traditional Chinese medicine compound in this embodiment, the XOD level in the mice was significantly downregulated, showing better results than the positive control group, suggesting that the traditional Chinese medicine compound in this embodiment can repair liver damage in hyperuricemia mice.

[0053] 3.5 Mouse liver tissue sections Experimental results show that ( Figure 5 In the blank control group, the liver lobule structure was intact, and the hepatocytes were morphologically normal and arranged radially. In the model group, the liver lobule structure was severely damaged, and inflammatory cell infiltration was observed in the hepatocyte interstitium (marked with arrows). Although the positive control group showed no obvious inflammation, the hepatic sinusoids were dilated, and the hepatocytes were irregularly arranged. In contrast, the experimental group had normal liver lobule structure, no obvious lesions, and some relief of hepatocyte damage. This demonstrates that hyperuricemia can cause hepatocyte damage, and the traditional Chinese medicine compound in this example improves uric acid-induced liver damage.

[0054] 3.6HK-2 cell kidney fibrosis gene TGF-β2 is the main indicator for assessing model establishment, while VIM, FN, COL1A1, and COL3A1 are common indicators for assessing the degree of fibrosis and are also downstream genes of the fibrosis pathway. Experimental results show ( Figure 6 Compared with the blank control group, the experimental group significantly upregulated the expression level of TGF-β2 in cells, suggesting that TGF-β can initiate the TGF-β / Smad signaling pathway and induce the upregulation of TGF-β2 expression in the pathway. Furthermore, in the experimental group after TGF-β induction of HK-2 cells, the expression of VIM, FN, COL1A1, and COL3A1 genes was significantly upregulated, while the experimental group significantly reduced the expression levels of these genes. This suggests that TGF-β induction can indeed cause fibrosis in renal tubular cells, and the traditional Chinese medicine compound in this example can improve the degree of fibrosis.

[0055] 3.7 Ankle swelling in rats Experimental results show that ( Figure 7 After modeling, the number of rats in both the model group and the experimental group increased significantly. After treatment with the traditional Chinese medicine compound in this embodiment, the ankle joint swelling of the rats in the experimental group was significantly reduced compared with that in the model group, suggesting that the traditional Chinese medicine compound in this embodiment can alleviate joint swelling caused by gouty arthritis.

[0056] 3.8 Inflammatory factors of rat ankle joints Experimental results show that ( Figure 8The expression levels of inflammatory factors IL-6, IL-1β, and TNF-α in the ankle joint tissue of the model group rats were increased. After treatment with the traditional Chinese medicine compound in this example, the expression of the three inflammatory factors in the tissue was significantly downregulated, indicating that the inflammatory response in the joint was weakened. The traditional Chinese medicine compound in this example can alleviate the increase of related factors caused by arthritis.

[0057] 3.9 Rats ankle joint sections Experimental results show that ( Figure 9 In the model group rats, severe proliferation of synovial cells was observed in the ankle joint tissue. The connective tissue beneath the synovial cells became dense due to collagen fiber proliferation, and there was extensive infiltration of lymphocytes and proliferation of fibroblasts within the synovium. After treatment with the traditional Chinese medicine compound in this example, the synovial structure near the ankle joint was improved, and inflammatory cell infiltration and collagen fiber proliferation were less observed in the interstitium.

[0058] All other parts not described in detail are existing technologies. Although the above embodiments have provided a detailed description of the present invention, they are only some embodiments of the present invention, not all embodiments. People can obtain other embodiments based on these embodiments without creative effort, and these embodiments all fall within the protection scope of the present invention.

Claims

1. A traditional Chinese medicine compound with medicinal and edible properties that has therapeutic effects on uric acid disorders, characterized in that: The raw materials of the Chinese herbal compound are all food and medicine homologous, and by weight, they include 15-25 parts of plantain seed, 15-25 parts of papaya, 5-15 parts of smilax glabra, 5-15 parts of purslane, 1-11 parts of prepared licorice root, 5-15 parts of mulberry leaf, 5-15 parts of perilla leaf, 1-11 parts of apricot kernel, 5-15 parts of polygonatum rhizome, 1-11 parts of black date, and 1-9 parts of mulberry fruit.

2. The medicinal and edible herbal compound formula for treating uric acid diseases according to claim 1, characterized in that: The raw materials of the Chinese herbal compound are all food and medicine homologous, and by weight, they include 17-23 parts of plantain seed, 17-23 parts of papaya, 7-13 parts of smilax glabra, 7-13 parts of purslane, 3-9 parts of prepared licorice root, 7-13 parts of mulberry leaf, 7-13 parts of perilla leaf, 3-9 parts of apricot kernel, 3-9 parts of polygonatum, 3-9 parts of black dates, and 1-7 parts of mulberry.

3. The medicinal and edible herbal compound formula for treating uric acid diseases according to claim 1, characterized in that: The raw materials of the Chinese herbal compound are all food and medicine homologous, and by weight, they include 20 parts of plantain seed, 20 parts of papaya, 10 parts of smilax glabra, 10 parts of purslane, 6 parts of prepared licorice root, 10 parts of mulberry leaf, 10 parts of perilla leaf, 6 parts of apricot kernel, 10 parts of polygonatum, 6 parts of black dates, and 4 parts of mulberry.

4. A method for preparing a traditional Chinese medicine compound with therapeutic effects on uric acid diseases as described in any one of claims 1 to 3, characterized in that: Includes the following steps: 1) Weigh out the following ingredients according to the above weight ratio: plantain seed, papaya, smilax glabra, purslane, prepared licorice root, mulberry leaf, perilla leaf, apricot kernel, polygonatum, black date, and mulberry. Soak them in water, heat over high heat until boiling, then simmer over low heat for 25 minutes. Pour out the first decoction, add water again and heat for 15 minutes to obtain the second decoction. 2) Mix the two solutions to obtain a traditional Chinese medicine compound.

5. The use of a traditional Chinese medicine compound with therapeutic effects on uric acid diseases as described in any one of claims 1 to 3 in the preparation of traditional Chinese medicine preparations for hyperuricemia-induced kidney damage and gouty arthritis.

6. A traditional Chinese medicine preparation, characterized in that: The traditional Chinese medicine preparation comprises the traditional Chinese medicine complex according to any one of claims 1 to 3 and pharmaceutically acceptable excipients.

7. The traditional Chinese medicine preparation according to claim 6, characterized in that: The excipients are any one or more of vitamin C, sorbitol, mannitol, xylitol, fructose, amino acids, meglumine, dextrin, magnesium stearate, sucrose, and citric acid.

8. The traditional Chinese medicine preparation according to claim 6 or 7, characterized in that: The traditional Chinese medicine preparation is any one of the following: powder, oral liquid, granule, tablet, capsule, pill, syrup, and ointment.

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