Use of low molecular weight pachyman in preparation of medicine for simultaneously relieving hyperuricemia and liver and kidney injury

Abstract

The application discloses application of low-molecular pachyman in preparation of a medicine for simultaneously relieving hyperuricemia and liver and kidney injury, and belongs to the technical field of biological medicine. The application finds through experiments that the low-molecular pachyman has good uric acid lowering effect, and the cytotoxicity result shows that the low-molecular pachyman (0-2000 mu g / mL) has no significant toxicity to liver and kidney cells; meanwhile, the application also finds that the low-molecular pachyman can relieve liver and kidney injury caused by allopurinol and benzbromarone when lowering uric acid. Therefore, the low-molecular pachyman in the application has a good application prospect in relieving hyperuricemia caused by oxypurinol and antagonizing liver and kidney injury caused by drugs.

Description

Technical Field

[0001] This invention relates to the field of biomedical technology, and in particular to the application of low molecular weight Poria cocos polysaccharide in the preparation of drugs that simultaneously alleviate hyperuricemia and liver and kidney damage. Background Technology

[0002] Hyperuricemia (HUA) is a chronic metabolic disease characterized by excessive uric acid in the blood, caused by purine metabolism disorders. Uric acid in the body is divided into two types: endogenous uric acid accounts for about one-third of the total, while exogenous uric acid accounts for about two-thirds. The raw materials for the synthesis of exogenous uric acid come from foods high in purines in the diet. Excessive or prolonged consumption of purine-rich foods, or foods that may raise purine levels in the body, will continuously increase the amount of uric acid produced, leading to hyperuricemia and even gout. With the gradual adjustment of lifestyles and dietary structures in humans and animals, the risk of chronic kidney disease, cardiovascular disease, and various metabolic diseases has greatly increased. Therefore, alleviating HUA caused by exogenous diet is an urgent and significant task for protecting the health of humans and animals.

[0003] Currently, chemical drugs have shown significant efficacy in treating hyperuricemia (HUA) in clinical practice, but they also have varying degrees of toxic side effects. HUA treatment drugs are broadly classified into two categories based on their mechanism of action: those that inhibit uric acid production and those that increase uric acid excretion. Drugs that inhibit uric acid production, such as allopurinol, reduce uric acid production by inhibiting xanthine oxidase, a key enzyme in uric acid production. However, with its increasingly widespread clinical application, serious toxic side effects have become increasingly apparent. Studies have shown that allopurinol may cause severe allergic reactions, often accompanied by leukocytosis, eosinophilia, and abnormal liver and kidney function. Drugs that increase uric acid excretion, such as benzbromarone, selectively inhibit the reabsorption of urate by the uric acid transport-related proteins URAT1 and GLUT9 in renal tubular epithelial cells, thereby lowering uric acid. Studies have also shown that benzbromarone has serious toxic side effects; for example, it can cause damage to hepatocyte mitochondria, inducing apoptosis and necrosis. Its metabolite, 5,6-dihydroxybenzbromarone, can also be oxidized to the hepatotoxic intermediate o-phenylalanine. Therefore, while these clinical uric acid-lowering drugs have good clinical efficacy, their high cost and severe toxic side effects cannot be ignored. Thus, given the severe liver and kidney toxicity associated with the use of conventional uric acid-lowering drugs in treating hyperuricemia (HUA), it is urgent to actively seek and develop uric acid-lowering drugs that are both effective and safe with no toxic side effects.

[0004] The low molecular weight water-soluble Poria cocos polysaccharide (WPCP) used in this invention is a water-soluble Poria cocos polysaccharide extracted from alkali-soluble Poria cocos polysaccharide through bioprocessing. Its molecular weight range has been determined to be 10,000-50,000 Da, and it exhibits good water solubility. Currently, there are no reports of WPCP within this molecular weight range being able to treat hyperuricemia caused by potassium oxonate while simultaneously antagonizing liver and kidney damage induced by allopurinol (AP) / benzbromarone (BZ). Summary of the Invention

[0005] The purpose of this invention is to provide the application of low molecular weight Poria cocos polysaccharide in the preparation of drugs that simultaneously alleviate hyperuricemia and liver and kidney damage, in order to solve the problems existing in the prior art. Low molecular weight Poria cocos polysaccharide can reduce the high uric acid level in the blood caused by potassium oxonate. At the same time, when used in combination with allopurinol or benzbromarone, it can alleviate the weight loss and liver and kidney damage in mice caused by allopurinol or benzbromarone while lowering uric acid. This shows that low molecular weight Poria cocos polysaccharide has a good application prospect in alleviating hyperuricemia caused by potassium oxonate and antagonizing liver and kidney damage caused by allopurinol or benzbromarone.

[0006] To achieve the above objectives, the present invention provides the following solution:

[0007] This invention provides the application of low molecular weight Poria cocos polysaccharide in the preparation of drugs to relieve hyperuricemia, wherein the molecular weight of the low molecular weight Poria cocos polysaccharide is 10,000-50,000 Daltons.

[0008] Preferably, the hyperuricemia is caused by potassium oxonate.

[0009] This invention also provides the application of low molecular weight Poria cocos polysaccharide in the preparation of drugs that simultaneously alleviate hyperuricemia and antagonize liver and kidney damage caused by drugs, wherein the molecular weight of the low molecular weight Poria cocos polysaccharide is 10,000-50,000 Daltons.

[0010] Preferably, the drugs for reducing side effects or toxicity include allopurinol and benzbromarone. More preferably, the liver and kidney damage caused by allopurinol is indicated by elevated biochemical indicators of liver and kidney function in mice.

[0011] Preferably, the hyperuricemia is caused by potassium oxonate.

[0012] The present invention also provides a drug for relieving hyperuricemia caused by potassium oxonate, wherein the drug has low molecular weight Poria cocos polysaccharide as the main active ingredient, and the molecular weight of the low molecular weight Poria cocos polysaccharide is 10,000-50,000 Daltons.

[0013] The present invention also provides a drug that simultaneously relieves hyperuricemia and antagonizes liver and kidney damage caused by antagonistic drugs, wherein the drug has low molecular weight Poria cocos polysaccharide as the main active ingredient, and the molecular weight of the low molecular weight Poria cocos polysaccharide is 10,000-50,000 Daltons;

[0014] The antagonistic drugs include allopurinol and benzbromarone;

[0015] The hyperuricemia mentioned above is caused by potassium oxonate.

[0016] Preferably, the drug further includes pharmaceutically acceptable excipients. The dosage form of the drug includes tablets, granules, capsules, powders, or oral liquids.

[0017] In this invention, potassium oxonate-induced hyperuricemia includes elevated blood uric acid levels, increased xanthine oxidase activity, and / or elevated or decreased transcription levels of uric acid transport-related genes caused by potassium oxonate. The aforementioned changes in the transcription levels of uric acid transport-related genes include elevated transcription levels of GLUT9 and URAT1, genes related to uric acid reabsorption, and decreased transcription levels of OAT1, a gene related to uric acid excretion.

[0018] The present invention discloses the following technical effects:

[0019] The WPCP extracted in this invention has a molecular weight of 10,000-50,000 Daltons and good water solubility. Cell experiments showed that WPCP at concentrations of 0-2000 μg / mL had no significant cytotoxicity and did not affect the growth of hepatocytes and kidney cells. Animal experiments showed that WPCP at a concentration of 250 mg / kg bw could reduce high uric acid levels in the blood of mice without hepatotoxicity or nephrotoxicity. Therefore, WPCP could be a new option for preparing drugs to alleviate hyperuricemia induced by potassium oxonate. Furthermore, the combined use of WPCP and AP / BZ could antagonize AP / BZ-induced liver and kidney damage in mice. Therefore, WPCP can be used in combination to antagonize organ damage caused by other uric acid-lowering drugs. The water-soluble low-molecular-weight Poria cocos polysaccharide of this invention has a promising application prospect in alleviating potassium oxonate-induced hyperuricemia while antagonizing drug-induced liver and kidney damage, laying a theoretical foundation for the preparation of drugs for the effective treatment of hyperuricemia without damaging liver and kidney function. Attached Figure Description

[0020] To more clearly illustrate the technical solutions in the embodiments of the present invention or the prior art, the drawings used in the embodiments will be briefly introduced below. Obviously, the drawings described below are only some embodiments of the present invention. For those skilled in the art, other drawings can be obtained based on these drawings without creative effort.

[0021] Figure 1 The effect of WPCP on the viability of AML12 cells (A) and PK15 cells (B);

[0022] Figure 2 The effect of WPCP on potassium oxonate-induced hyperuricemia in the blood;

[0023] Figure 3The effects of WPCP or WPCP combined with AP / BZ on liver and kidney function in mice;

[0024] Figure 4 The effect of WPCP or WPCP combined with AP / BZ on XOD activity in mouse liver;

[0025] Figure 5 To detect the effect of WPCP on the transcriptional level of uric acid transport-related genes induced by potassium oxonate using RT-qPCR. Detailed Implementation

[0026] Various exemplary embodiments of the present invention will now be described in detail. This detailed description should not be considered as a limitation of the present invention, but rather as a more detailed description of certain aspects, features, and embodiments of the present invention.

[0027] It should be understood that the terminology used in this invention is merely for describing particular embodiments and is not intended to limit the invention. Furthermore, with respect to numerical ranges in this invention, it should be understood that each intermediate value between the upper and lower limits of the range is also specifically disclosed. Any stated value or intermediate value within a stated range, as well as each smaller range between any other stated value or intermediate value within said range, is also included in this invention. The upper and lower limits of these smaller ranges may be independently included or excluded from the range.

[0028] Unless otherwise stated, all technical and scientific terms used herein have the same meaning as commonly understood by one of ordinary skill in the art. While only preferred methods and materials have been described herein, any methods and materials similar or equivalent to those described herein may be used in the implementation or testing of this invention. All references to this specification are incorporated by way of citation to disclose and describe methods and / or materials associated with those references. In the event of any conflict with any incorporated reference, the content of this specification shall prevail.

[0029] Various modifications and variations can be made to the specific embodiments described in this specification without departing from the scope or spirit of the invention, as will be apparent to those skilled in the art. Other embodiments derived from this specification will also be readily apparent to those skilled in the art. This specification and embodiments are merely exemplary.

[0030] The terms “include,” “including,” “have,” “contain,” etc., used in this article are all open-ended terms, meaning that they include but are not limited to.

[0031] The following examples involve some of the experimental materials:

[0032] (1) Cells

[0033] AML12 and PK15 cell lines: purchased from the China Center for Type Culture Collection.

[0034] (2) Reagents

[0035] Potassium oxazine: Product number P831461, purchased from Shanghai Maclean Biochemical Technology Co., Ltd.;

[0036] Allopurinol: Product No. A800424, purchased from Shanghai Maclean Biochemical Technology Co., Ltd.;

[0037] Benzbromarone: Product No. B838527, purchased from Shanghai Maclean Biochemical Technology Co., Ltd.;

[0038] DMEM high glucose medium: Product number SH30243, purchased from Thermo Fisher Scientific Biochemical Products Co., Ltd.;

[0039] Fetal bovine serum: Product number 10099-141C, purchased from Gibco;

[0040] CCK-8 reagent kit: Catalog number A311, purchased from Nanjing Novizan Biotechnology Co., Ltd.;

[0041] XOD test kit: Item No. A002-1-1, purchased from Nanjing Jiancheng Bioengineering Research Institute Co., Ltd.;

[0042] 2X Universal SYBR Green Fast qPCRMix: Product No. RK21203, purchased from Wuhan Aiboteke Biotechnology Co., Ltd.;

[0043] II 1st Strand cDNA Synthesis Kit (gDNAwiper): Product No. R212, purchased from Nanjing Novizan Biotechnology Co., Ltd.;

[0044] Chloroform: Product No. 10006818, purchased from China National Pharmaceutical Group Shanghai Chemical Reagent Company;

[0045] Isopropanol: Product No. 80109218, purchased from China National Pharmaceutical Group Shanghai Chemical Reagent Company;

[0046] Anhydrous ethanol: Product number 10009218, purchased from Sinopharm Chemical Reagent Co., Ltd.

[0047] (3) Preparation and identification of WPCP

[0048] Preparation of WPCP: Extracted via bioprocessing methods, the specific methods are as follows:

[0049] Poria polysaccharide was obtained by referring to "Liu Xin, Xiong Fangqi, Yu Qiansha, et al. Optimization of extraction process of Poria polysaccharide" and used as raw material for further separation and extraction.

[0050] Accurately weigh 26.6g of Poria cocos polysaccharide raw material, add 100mL of 50% peroxidase solution to the solution, mix thoroughly, and react for 1h. After heating the solution at 98℃ for 15min, remove it and let it cool to room temperature. Centrifuge at 1000r / min for 3min, collect the supernatant, and obtain water-soluble Poria cocos polysaccharide.

[0051] WPCP molecular weight determination:

[0052] Water-soluble low-molecular-weight Poria cocos polysaccharides were detected by high-performance liquid chromatography (with differential detector). Specific data are shown in Table 1, based on the molecular weight and molecular weight distribution detection method. Polysaccharides with a molecular weight less than 50,000 Daal accounted for 96.5%. The solubility in water reached 1:50, indicating good water solubility.

[0053] Table 1 Results of molecular weight and molecular weight distribution determination

[0054] Serial Number Molecular weight (Dal) Percentage (%) 1 ≥1 million 3.49 2 ≤50,000 96.50

[0055] Example 1: Toxicity of WPCP on AML12 and PK15 cells

[0056] 1. Drug treatment

[0057] AML12 cells (1×10) 4 The cells were seeded into 96-well plates, and after the cell density reached 70-80%, WPCP was added for 24 hours. The final WPCP concentrations were 25, 50, 100, 200, 500, 800, 1000, and 2000 μg / mL, with a drug volume of 100 μL per well. Each dose was used in 6 parallel wells, and a blank group (no cells, only culture medium) and a control group (cells, no drug) were also included.

[0058] The treatment method for PK15 cells is the same as above.

[0059] 2. CCK-8 assay for WPCP cytotoxicity

[0060] 24 hours after drug administration, the 96-well plates were removed for cytotoxicity testing. First, CCK-8 reagent was diluted with DMEM basal medium at a ratio of 1:10, and then 100 μL was added to each well. The 96-well plates were incubated at 37°C in a 5% CO2 cell culture incubator for 1 hour, and the absorbance (OD) was read at 450 nm using a microplate reader. 450 ).

[0061] Cell viability (%) = (Experimental group OD) 450 - Blank group OD450 ) / (control group OD 450 - Blank group OD 450 )*100.

[0062] 3. Results

[0063] Experimental results are as follows Figure 1 As shown, the results indicate that WPCP at concentrations of 0-2000 μg / mL did not exhibit significant cytotoxicity against AML12 and PK15 cells.

[0064] Example 2: Effect of WPCP on AP / BZ-induced body weight in mice

[0065] 1. Mouse treatment

[0066] Male Kunming mice were randomly divided into 11 groups: a blank control group (oral administration of equal volume of 0.5% sodium carboxymethyl cellulose + equal volume of 0.5% sodium carboxymethyl cellulose), a potassium oxonate group (oral administration of 200 mg / kg bw + equal volume of 0.5% sodium carboxymethyl cellulose), a potassium oxonate + AP group (oral administration of 200 mg / kg bw + 20 mg / kg bw), a potassium oxonate + BZ group (oral administration of 200 mg / kg bw + 10 mg / kg bw), a potassium oxonate + WPCP group (oral administration of 200 mg / kg bw + 250 mg / kg bw), a potassium oxonate + AP + WPCP-D group (oral administration of 200 mg / kg bw + 20 mg / kg bw + 250 mg / kg bw), and a potassium oxonate + AP + WPCP-Z group (oral administration of 200 mg / kg bw + 20 mg / kg bw). The following groups received oral oxonate (BW) via gavage, followed by WPCP / AP / BZ / 0.5% sodium carboxymethyl cellulose solution. All groups received potassium oxonate via gavage for 1 hour, followed by WPCP / AP / BZ / 0.5% sodium carboxymethyl cellulose solution.

[0067] 2. Measure weight

[0068] The experiment lasted for seven days. The mice were weighed on days 0, 1, 3, 5 and 7, and all data were statistically analyzed.

[0069] 3. Results

[0070] The weight gain of mice is shown in Table 2. 20 mg / kg b.w.AP or 10 mg / kg bwBZ significantly inhibited the weight gain of mice on days 1, 3, 5 and 7, resulting in slow growth. WPCP had no inhibitory effect on mouse growth, and the slow growth phenomenon in the combined drug group was significantly alleviated.

[0071] Table 2 Effects of WPCP or WPCP combined with AP / BZ on mouse weight gain

[0072]

[0073] Note: Compared with the control group, * indicates a significant difference (P < 0.05), and ** indicates an extremely significant difference (P < 0.01).

[0074] Example 3: Effect of WPCP on potassium oxonate-induced hyperuricemia in blood.

[0075] 1. Mouse treatment

[0076] Same as Example 2.

[0077] 2. Detect blood uric acid levels in different groups

[0078] After 7 days of experimentation, blood was collected from the orbital region of mice. The collected blood was centrifuged at 3000 rpm for 15 minutes, and the supernatant was used to detect the uric acid content on a fully automated biochemical analyzer.

[0079] 3. Results

[0080] The results of WPCP in reducing hyperuricemia in the blood caused by potassium oxonate are as follows: Figure 2 As shown in the results, compared with the control group, WPCP, AP, BZ and the combination therapy group all significantly reduced the blood uric acid level in mice.

[0081] Example 4: Effects of WPCP on AP / BZ-induced liver and kidney function damage

[0082] 1. Mouse treatment

[0083] Same as Example 2.

[0084] 2. Detection of the levels of liver and kidney function damage indicators induced by different groups of AP / BZ in mice.

[0085] After 7 days of experimentation, blood was collected from the orbital region of mice. The collected blood was centrifuged at 3000 rpm for 15 min, and the supernatant was used to detect the contents of ALT, AST, LDH, CREA, and UREA on a fully automated biochemical analyzer.

[0086] 3. Results

[0087] Blood biochemical results of WPCP in alleviating AP and BZ-induced liver and kidney function damage in mice are as follows: Figure 3 As shown, 20 mg / kg bwAP or 10 mg / kg bwBZ can cause abnormal increases in biochemical indicators of liver or kidney function in mice to varying degrees; while WPCP has no effect on liver or kidney function in mice, and the levels of ALT, AST, LDH, CREA, and UREA in the combined drug group are not significantly different from those in the control group, indicating that WPCP can significantly alleviate the liver and kidney function damage induced by AP / BZ in mice.

[0088] Example 5: Effect of WPCP on Hepatic XOD Activity

[0089] 1. Mouse treatment

[0090] Same as Example 2.

[0091] 2. Detection of liver XOD activity in different groups

[0092] After 7 days of experimentation, liver tissue from mice was collected and placed in 0.9% NaCl solution. The liver XOD activity was then measured according to the XOD test kit instructions.

[0093] 3. Results

[0094] The results of WPCP inhibiting hepatic XOD activity are as follows Figure 4 As shown in the results, compared with the control group, WPCP, AP, BZ and the combination therapy group all significantly inhibited liver XOD activity.

[0095] Example 6: Effects of WPCP on the transcriptional levels of renal uric acid transport-related genes

[0096] 1. Mouse treatment

[0097] Same as Example 2.

[0098] 2. Detection of transcription levels of renal uric acid transport-related genes in different groups

[0099] After 7 days of experimentation, an appropriate amount of mouse kidneys were collected and placed in 1.5 mL EP enzyme-free tubes for RT-qPCR detection. The RT-qPCR steps are as follows:

[0100] a. Tissue lysis: Add 1 mL of Trizol reagent to each tube, homogenize using a tissue homogenizer, let stand at room temperature for 5 min, centrifuge at 12000 r / min for 15 min at 4℃, and transfer the supernatant to a new 1.5 mL EP enzyme-free tube.

[0101] b. RNA isolation: Add 100 μL of chloroform (1 / 5 of the total Trizol volume) to a centrifuge tube containing the lysate, vortex for 30 seconds until the solution emulsifies and turns milky white, and let stand at room temperature for 5 minutes; centrifuge at 12000 rpm for 15 minutes at 4°C, separating into three layers. Upper layer: RNA (approximately 60% of Trizol); Middle layer: DNA; Lower layer: protein (phenol-chloroform); carefully aspirate the supernatant (using a 100 or 200 μL pipette) and transfer it to a new 1.5 mL enzyme-free EP tube. Do not aspirate the white middle layer. The volume of supernatant produced by 0.5 mL of lysate is approximately 200–300 μL.

[0102] c. RNA precipitation: Add approximately 250 μL (0.5–1 volume of Trizol) of isopropanol to the supernatant, invert the centrifuge tube to mix thoroughly, and incubate at room temperature for 10 min. Centrifuge at 12000 rpm for 10 min at 4°C. RNA precipitate will form on the side of the bottom of the centrifuge tube. Carefully aspirate the supernatant, taking care to avoid discarding the RNA precipitate.

[0103] d. RNA washing: Carefully discard the supernatant, slowly add 0.5 mL of pre-cooled 75% ethanol (anhydrous ethanol: DEPC H2O = 3:1) along the wall of the EP tube, gently invert the tube to wash the wall, centrifuge at 12000 r / min for 5 min at 4℃, and then carefully discard as much ethanol as possible; repeat the above washing steps once.

[0104] e. RNA dissolution: Dry the precipitate at room temperature for 3-5 minutes. Add 200 μL of DEPC H2O to each EP tube to dissolve the precipitate. If necessary, gently pipette the precipitate. After the RNA precipitate is completely dissolved, store at -80℃.

[0105] f. RNA quality and purity detection: Take 1 μL of total RNA sample and detect the RNA concentration and A in a Q3000 spectrophotometer. 260 / A 280 The ratio can be used to determine the purity of the extracted RNA; a ratio between 1.8 and 2.0 is considered acceptable.

[0106] g. RNA reverse transcription to cDNA: The extracted total RNA samples were strictly processed according to Vazyme's... The instructions for the III RTSuperMix for qPCR (+gDNAwiper) reverse transcription method state that subsequent experiments should be performed using RT-qPCR.

[0107] h. RT-qPCR detection of gene expression: The coding region sequence of the target gene was searched on NCBI-Pubmed. To ensure specificity, the primers should be located within the 300-400 bp region at the 5' end of the coding region published by NCBI. When designing primers using NCBI-Primer software, the amplification product length should not exceed 300 bp, dimers should not form, the G+C content in the primers should be approximately 55%, there should be no more than four consecutive complementary structures within or between primers, and the primer Tm value should be 55-65℃. The designed primers were synthesized by Sangon Biotech (Shanghai) Co., Ltd. The synthesized primers were dissolved in 500 μL of enzyme-free water according to the instructions to a primer concentration of 10 μM. The reaction mixture was vortexed, centrifuged, and then aliquoted into 96-well plates. The plates were centrifuged on a centrifuge and then subjected to thermal cycling on a Bio-Rad CFX96 RT-PCR instrument. After the thermal cycling reaction, the amplification curves and melting curves of each gene were analyzed for result analysis. Following the Ibotek 2X Universal SYBR Green FastqPCR Mix PCR quantitative reaction system, the total system volume was 10 μL. The starting point for cDNA to enter the exponential growth phase of PCR, i.e., the cycle threshold (Ct), was determined by the system analysis software after the RT-qPCR reaction, thus determining the Ct value of each reaction sample. The Ct value was then determined using the Ct comparison method, i.e., 2... -ΔΔCt To calculate gene expression levels.

[0108] The calculation formula is: Folds = 2 -ΔΔCt , △△Ct=(Ctl-Ct2)-(Ct3-Ct4).

[0109] Ct1: Critical cycle number for the target gene in the treatment sample; Ct2: Critical cycle number for the housekeeping gene in the treatment sample; Ct3: Critical cycle number for the target gene in the control sample; Ct4: Critical cycle number for the housekeeping gene in the control sample. 2 -ΔΔCt This indicates the fold change in the expression level of the target gene in the experimental group relative to the control group.

[0110] 3. Results

[0111] The results of WPCP inhibiting the increase / decrease in the transcriptional levels of renal uric acid transport-related genes are as follows: Figure 5As shown in the results, compared with the control group, the oxonate group had significantly increased GLUT9 and URAT1 gene transcription levels and significantly decreased OAT1 gene transcription levels, suggesting that oxonate increases uric acid levels by affecting the transcription levels of uric acid transport-related genes. Meanwhile, WPCP, AP, BZ, and the combined drug group all significantly reduced the increase in transcription levels of uric acid reabsorption-related genes GLUT9 and URAT1 in the kidneys. Simultaneously, WPCP significantly increased the transcription level of uric acid secretion-related gene OAT1, suggesting that WPCP may exert its uric acid-lowering effect by simultaneously reducing uric acid reabsorption and increasing uric acid excretion.

[0112] The embodiments described above are merely preferred embodiments of the present invention and are not intended to limit the scope of the present invention. Various modifications and improvements made by those skilled in the art to the technical solutions of the present invention without departing from the spirit of the present invention should fall within the protection scope defined by the claims of the present invention.

Claims

1. The application of low molecular weight Poria cocos polysaccharide in the preparation of drugs that simultaneously alleviate hyperuricemia and reduce liver and kidney damage caused by allopurinol or benzbromarone, characterized in that, The molecular weight of the low-molecular-weight Poria cocos polysaccharide is 10,000-50,000 Daltons.

2. The application as described in claim 1, characterized in that, The drug also includes pharmaceutically acceptable excipients.

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