Application of pediococcus pentosaceus A21243 in reducing blood uric acid and improving renal function

Abstract

The invention belongs to the technical field of functional microorganisms, discloses application of pediococcus pentosaceus A21243 in reducing blood uric acid and improving renal functions, and provides application of the pediococcus pentosaceus A21243 in preparing products for preventing or treating nephropathy and hyperuricemia, the pediococcus pentosaceus is the pediococcus pentosaceus A21243, and the preservation number is GDMCC NO: 63749. The Pediococcus pentosaceus A21243 has the effects of improving and delaying renal insufficiency caused by hyperuricemia, hyperglycemia and cis-platinum, and meanwhile, the Pediococcus pentosaceus A21243 can also promote excretion of uric acid through intestinal feces by inhibiting the activity of purine metabolism related enzymes in a uric acid generation pathway, such as the activity of xanthine oxidase (XOD), purine nucleoside phosphorylase (PNP) and adenosine deaminase (ADA), so that the Pediococcus pentosaceus A21243 can be used for improving and delaying renal insufficiency caused by hyperuricemia, hyperglycemia and cis-platinum. The oxidative stress disorder caused by high uric acid is regulated, so that the beneficial effect of reducing blood uric acid is achieved.

Description

Technical Field

[0001] The invention belongs to the technical field of functional microorganisms, and specifically relates to application of Pediococcus pentosaceus A21243 in reducing blood uric acid and improving renal function. Background Art

[0002] Hyperuricemia (HUA) is a chronic metabolic disease caused by elevated blood uric acid levels due to purine metabolism disorders or uric acid excretion disorders in the body. It is prone to cause gouty acute arthritis attacks, tophi deposition, tophi chronic arthritis and joint deformities. It often affects the kidneys and causes chronic interstitial nephritis and uric acid kidney stone formation. The causes of hyperuricemia are usually divided into two types: increased uric acid production and decreased uric acid excretion. Factors that lead to increased uric acid production include high levels of purines in the diet and increased purine metabolism; the causes of decreased uric acid excretion are mostly related to kidney disease, and also include some drug factors and competitive excretion between uric acid and other molecules.

[0003] The current treatment direction of HUA is mainly to reduce the excessive production of urate or increase renal and / or gastrointestinal excretion or both. Methods include drug therapy and non-drug therapy, but both have adverse reactions. Among them, the drugs used in clinical practice are mainly uricosuric drugs, uric acid inhibitors and alkaline drugs, which relieve hyperuricemia by increasing uric acid excretion, inhibiting uric acid production or alkalizing urine. Insufficient urate excretion is the main cause of gout hyperuricemia. Dietary factors can also greatly affect the production of urate. In addition, the burden of gout is aggravated by the additional impact of complications that are prevalent in gout patients, including hypertension (75%), chronic kidney disease (CKD) (70%), obesity (53%) and cardiovascular disease (CVD) (10% to 14%), which are associated with increased morbidity and mortality risks. The incidence of metabolic syndrome is also higher in gout patients, and asymptomatic hyperuricemia is more common in patients with metabolic syndrome, which seriously endangers people's health. Based on the defects and shortcomings of existing treatment methods, there is an urgent need to seek an effective, stable, safe and convenient HUA treatment strategy.

[0004] With the improvement of living standards, changes in lifestyle and aging of the population in my country, the incidence of metabolic diseases such as diabetes, hypertension, obesity, hyperuricemia and gout has gradually increased, leading to an increase in the incidence of secondary kidney disease year by year. Continuous high blood sugar can lead to glomerular sclerosis, lesions of renal arterioles and glomerular capillary filtration membranes, and is the pathological basis for proteinuria and renal insufficiency. Sodium urate crystals deposited in the renal medulla can lead to chronic tubulointerstitial nephritis, renal fibrosis, and urinary tract stones and obstruction.

[0005] Pediococcus pentosaceus, a species of Lactobacillus, plays an important role in food production, storage and promoting human health.

[0006] To date, issues related to the practical application of Pediococcus pentosaceus as a probiotic remain unresolved, for example, there is a lack of knowledge about mechanisms, side effects, usage, and dosage. Increasing evidence suggests that Pediococcus pentosaceus and its metabolites perform well in the food industry and intestinal health. At present, the screening indicators of Lactobacillus strains, the in vivo effects and mechanisms of regulating blood uric acid are still unclear, and there are relatively few reports on the improvement of hyperuricemia by Pediococcus pentosaceus. Therefore, screening Pediococcus pentosaceus that can lower uric acid and improve metabolic kidney diseases such as hyperuricemia, hyperglycemia, and hyperlipidemia is of great significance for the treatment of hyperuricemia and the research of drugs targeting hyperuricemia. Summary of the invention

[0007] The present invention aims to overcome the shortcomings of the prior art and provides a strain of Pediococcus pentosaceus derived from fecal samples of centenarians in Guangxi, which has the effects of lowering uric acid or protecting the kidneys and improving renal function, and its postbiotic application. It is found that the strain has the ability to degrade uric acid in vitro and regulate oxidative stress disorders in intestinal hyperuricemia model mice, and can effectively reduce uric acid, and can be used to treat hyperuricemia and renal insufficiency.

[0008] The purpose of the first aspect of the present invention is to provide the use of Pediococcus pentosaceus A21243 or its products in the preparation of products for preventing or treating kidney disease.

[0009] The second aspect of the present invention aims to provide the use of Pediococcus pentosaceus A21243 or its products in the preparation of products for preventing or treating hyperuricemia.

[0010] In order to achieve the above object, the technical solution adopted by the present invention is:

[0011] The first aspect of the present invention provides the use of Pediococcus pentosaceus A21243 or a product thereof in the preparation of a product for preventing or treating kidney disease, wherein the deposit number of the Pediococcus pentosaceus A21243 is GDMCC NO:63749.

[0012] The taxonomic name of Pediococcus pentosaceus A21243 was Pediococcus pentosaceus and it was deposited in Guangdong Provincial Microbiological Culture Collection Center on August 24, 2023.

[0013] In some embodiments of the present invention, the kidney disease includes renal insufficiency caused by diabetes, hyperuricemia, and cisplatin.

[0014] In some embodiments of the invention, the treatment includes alleviation or improvement.

[0015] In some embodiments of the present invention, the diabetes comprises type 2 diabetes.

[0016] In some embodiments of the present invention, the product includes at least one of a probiotic preparation containing Pediococcus pentosaceus A21243, a microcapsule, a solid beverage, a fermented milk, and a lactic acid bacteria beverage.

[0017] In some embodiments of the present invention, the probiotic preparation containing Pediococcus pentosaceus A21243 includes a lyophilized bacterial preparation, and the preparation method thereof includes the following steps:

[0018] The Pediococcus pentosaceus strain A21243 is activated and inoculated into an MRS liquid culture medium under anaerobic conditions for culture. The obtained seed liquid is expanded and cultured, and then the bacterial bodies are collected. The bacterial bodies are mixed with a freeze-drying protective agent and then freeze-dried to obtain freeze-dried bacterial powder.

[0019] In some preferred embodiments of the present invention, the culturing under anaerobic conditions preferably includes static culturing, and the culturing time is 10 to 13 hours.

[0020] In some preferred embodiments of the present invention, the number of times of culturing under anaerobic conditions includes 2 to 3 times.

[0021] In some preferred embodiments of the present invention, the culture temperature is 36-38°C, more preferably 37°C.

[0022] In some preferred embodiments of the present invention, the expanded culture is carried out under anaerobic conditions at 37° C. for 20 to 24 hours.

[0023] In some preferred embodiments of the present invention, the method for collecting bacteria is centrifugation. The speed of the centrifugation is preferably 5000 rpm, and the time of the centrifugation is 5 min.

[0024] In some preferred embodiments of the present invention, the bacterial cells are washed with physiological saline and then mixed with a lyophilization protective agent.

[0025] In some preferred embodiments of the present invention, the lyoprotectant comprises skim milk powder and trehalose, and the lyoprotectant is obtained by mixing a skim milk powder solution having a mass concentration of 10% to 12% and a trehalose having a mass concentration of 10% to 12% in a volume ratio of 1:1.

[0026] In some embodiments of the present invention, the microcapsule containing Pediococcus pentosaceus A21243 comprises a core material, a wall material and a cross-linking agent.

[0027] In some preferred embodiments of the present invention, the core material includes Pediococcus pentosaceus A21243, which is prepared by the following method: Pediococcus pentosaceus A21243 is planted in MRS liquid culture medium, and statically cultured under anaerobic conditions at 35-38°C for 20-24 hours to obtain a cultured bacterial liquid, and the bacterial cells are collected by centrifugation and washed with physiological saline, and centrifuged to obtain the bacterial cells, that is, the core material.

[0028] In some preferred embodiments of the present invention, the wall material includes sodium alginate and modified starch, and is prepared by the following method: 1% to 3% sodium alginate aqueous solution and 1% to 3% modified starch aqueous solution are sterilized and then mixed evenly in a volume ratio of 1:1 to 3 to obtain the wall material.

[0029] In some preferred embodiments of the present invention, the cross-linking agent comprises calcium chloride.

[0030] In some preferred embodiments of the present invention, the method for preparing the microcapsules comprises the following steps: mixing the wall material and the core material, spraying them into a crosslinking agent calcium chloride (1% to 2%, m / V) solution after atomization through a spray nozzle, allowing calcium ions to crosslink with sodium hyaluronate to form microcapsules, and statically curing for 110 to 130 minutes to obtain microcapsules.

[0031] In some embodiments of the present invention, the solid beverage containing Pediococcus pentosaceus A21243 includes, by mass percentage, 30% to 45% whole milk powder, 8% to 12% fructooligosaccharide, 8% to 12% trehalose, 8% to 12% freeze-dried powder of Pediococcus pentosaceus A21243 strain, 8% to 12% whey protein powder, 3% to 6% citric acid, 3% to 6% maltodextrin, 3% to 6% carrageenan, and 3% to 6% edible flavor. The preparation method of the solid beverage comprises mixing the above ingredients evenly to obtain the solid beverage.

[0032] In some embodiments of the present invention, the method for preparing fermented milk containing Pediococcus pentosaceus A21243 comprises the following steps: adding Pediococcus pentosaceus A21243 in an amount of 1% to 2% (m / V) to the formulated, homogenized and sterilized cow's milk, fermenting at 38 to 42° C. for 20 to 26 hours, and adding the obtained fermentation liquid as a seed liquid to new cow's milk in an amount of 1% to 3%, fermenting at 8 to 42° C. for 20 to 26 hours, and refrigerating at 3 to 5° C. for 20 to 26 hours to obtain fermented milk containing Pediococcus pentosaceus A21243.

[0033] In some embodiments of the present invention, the viable count of Pediococcus pentosaceus A21243 in the fermented milk is greater than 1.0×10 9 CFU / mL.

[0034] In some embodiments of the present invention, the preparation method of the lactic acid bacteria beverage containing Pediococcus pentosaceus A21243 comprises the following steps: inoculating Pediococcus pentosaceus A21243 at an inoculation rate of 4% to 6% into a sterile mixed solution containing soy milk, cheese whey and sucrose, and fermenting at 38 to 42° C. for 20 to 26 hours to obtain a lactic acid bacteria beverage containing Pediococcus pentosaceus A21243.

[0035] In some embodiments of the present invention, the product includes food and medicine.

[0036] In some embodiments of the present invention, the dosage form of the drug is selected from tablets (such as ordinary tablets, double-layer tablets, multi-layer tablets, sustained-release tablets, single-chamber controlled-release tablets, double-chamber controlled-release tablets, microporous controlled-release tablets, dispersible tablets, enteric-coated tablets), pills, powders, suspensions, gels, emulsions, creams, granules, nanoparticles, capsules (such as ordinary capsules, sustained-release capsules, controlled-release capsules, capsules containing micropellets or small tablets, pH-dependent capsules containing micropellets or small tablets, gastrointestinal composite capsules), suppositories, injections, sprays and injections.

[0037] In some embodiments of the present invention, the product further comprises a pharmaceutically acceptable excipient.

[0038] In some embodiments of the present invention, the pharmaceutically acceptable excipients include at least one of fillers, disintegrants, diluents, dispersants, excipients, stabilizers, lubricants, binders, wetting agents, flavoring agents, suspending agents, solvents, sustained-release agents, emulsifiers, absorption enhancers, surfactants, preservatives, pigments, flavors and solvents.

[0039] In some embodiments of the present invention, the filler is selected from starch, sucrose, lactose, mannitol, sorbitol, xylitol, microcrystalline cellulose or glucose; the binder is selected from cellulose derivatives, alginate, starch, water, dextrin, gelatin or polyvinyl pyrrolidone; the disintegrant is selected from microcrystalline cellulose, sodium methyl starch, cross-linked polyvinyl pyrrolidone, low-substituted hydroxypropyl cellulose or cross-linked sodium methyl cellulose; the lubricant is selected from stearic acid, polyethylene glycol, calcium carbonate, sodium bicarbonate, micro-powder silica gel, talc or magnesium stearate; the suspending agent is selected from micro-powder silica gel, beeswax, cellulose, solid polyethylene glycol : The wetting agent is selected from glycerol, Tween-80, hydrogenated castor oil or lecithin; the solvent is selected from ethanol, liquid polyethylene glycol, isopropanol, Tween-80, glycerol, propylene glycol or vegetable oil, and the vegetable oil is selected from soybean oil, castor oil, peanut oil, blending oil, etc.; the surfactant is selected from sodium dodecylbenzene sulfonate, stearic acid, polyoxyethylene-polyoxypropylene copolymer, fatty acid sorbitan or polysorbate (Tween), etc.; the flavoring agent is selected from aspartame, sucralose, flavor, stevioside, acesulfame potassium, citric acid or saccharin sodium; the preservative is selected from at least one of methyl paraben or propyl paraben.

[0040] In some embodiments of the present invention, the bacterial count of Pediococcus pentosaceus A21243 in the product is greater than 10 7 CFU.

[0041] The second aspect of the present invention provides the use of Pediococcus pentosaceus A21243 or a product thereof in the preparation of a product for preventing or treating hyperuricemia, wherein the deposit number of Pediococcus pentosaceus A21243 is GDMCC NO:63749.

[0042] In some embodiments of the present invention, the drug achieves the purpose of preventing or treating hyperuricemia by reducing the uric acid content in the subject's serum, inhibiting the activity of xanthine oxidase, purine nucleoside phosphorylase and / or adenosine deaminase in the subject's liver, regulating the subject's oxidative stress disorder and promoting the subject's excretion of uric acid.

[0043] In some embodiments of the present invention, regulating the oxidative stress disorder in the subject comprises regulating the levels of SOD, CAT, GSH and MDA in the liver of the subject.

[0044] In some embodiments of the present invention, the product includes at least one of a probiotic preparation containing Pediococcus pentosaceus A21243, a microcapsule, a solid beverage, a fermented milk, and a lactic acid bacteria beverage.

[0045] In some embodiments of the present invention, the product includes food and medicine.

[0046] In some embodiments of the present invention, the dosage form of the drug is selected from tablets (such as ordinary tablets, double-layer tablets, multi-layer tablets, sustained-release tablets, single-chamber controlled-release tablets, double-chamber controlled-release tablets, microporous controlled-release tablets, dispersible tablets, enteric-coated tablets), pills, powders, suspensions, gels, emulsions, creams, granules, nanoparticles, capsules (such as ordinary capsules, sustained-release capsules, controlled-release capsules, capsules containing micropellets or small tablets, pH-dependent capsules containing micropellets or small tablets, gastrointestinal composite capsules), suppositories, injections, sprays and injections.

[0047] In some embodiments of the present invention, the product further comprises a pharmaceutically acceptable excipient.

[0048] In some embodiments of the present invention, the pharmaceutically acceptable excipients include at least one of fillers, disintegrants, diluents, dispersants, excipients, stabilizers, lubricants, binders, wetting agents, flavoring agents, suspending agents, solvents, sustained-release agents, emulsifiers, absorption enhancers, surfactants, preservatives, pigments, flavors and solvents.

[0049] In some embodiments of the present invention, the filler is selected from starch, sucrose, lactose, mannitol, sorbitol, xylitol, microcrystalline cellulose or glucose; the binder is selected from cellulose derivatives, alginate, starch, water, dextrin, gelatin or polyvinyl pyrrolidone; the disintegrant is selected from microcrystalline cellulose, sodium methyl starch, cross-linked polyvinyl pyrrolidone, low-substituted hydroxypropyl cellulose or cross-linked sodium methyl cellulose; the lubricant is selected from stearic acid, polyethylene glycol, calcium carbonate, sodium bicarbonate, micro-powder silica gel, talc or magnesium stearate; the suspending agent is selected from micro-powder silica gel, beeswax, cellulose, solid polyethylene glycol : The wetting agent is selected from glycerol, Tween-80, hydrogenated castor oil or lecithin; the solvent is selected from ethanol, liquid polyethylene glycol, isopropanol, Tween-80, glycerol, propylene glycol or vegetable oil, and the vegetable oil is selected from soybean oil, castor oil, peanut oil, blending oil, etc.; the surfactant is selected from sodium dodecylbenzene sulfonate, stearic acid, polyoxyethylene-polyoxypropylene copolymer, fatty acid sorbitan or polysorbate (Tween), etc.; the flavoring agent is selected from aspartame, sucralose, flavor, stevioside, acesulfame potassium, citric acid or saccharin sodium; the preservative is selected from at least one of methyl paraben or propyl paraben.

[0050] The beneficial effects of the present invention are:

[0051] The present invention provides the use of Pediococcus pentosaceus A21243 in the preparation of products for preventing or treating nephropathy and hyperuricemia, wherein the Pediococcus pentosaceus is Pediococcus pentosaceus A21243, and the deposit number is: GDMCC NO: 63749. The Pediococcus pentosaceus A21243 in the present invention has the effects of improving and delaying metabolic renal insufficiency caused by hyperuricemia and hyperglycemia, and renal insufficiency caused by cisplatin, and at the same time, the strain can also inhibit the activity of purine metabolism-related enzymes in the uric acid production pathway, such as inhibiting the activity of xanthine oxidase (XOD), purine nucleoside phosphorylase (PNP), and adenosine deaminase (ADA), promote the excretion of uric acid through intestinal feces, regulate the oxidative stress disorder caused by hyperuricemia, etc., to achieve the beneficial effect of reducing blood uric acid. It has extremely high development value and practical value, and provides new ideas for the development and application of related products. BRIEF DESCRIPTION OF THE DRAWINGS

[0052] Figure 1 The serum uric acid concentrations of mice in each group before (0 day) and after (28 days) intervention with different doses of A21243. In the figure, ns represents no significant difference, ** represents P < 0.01, *** represents P < 0.001, and **** represents P < 0.0001.

[0053] Figure 2 Figure 3 Changes of serum uric acid in HUA mice during intervention with different doses of A21243.

[0054] Figure 3 The inhibitory effect of A21243 on the activities of xanthine oxidase (XOD), purine nucleoside phosphorylase (PNP), and adenosine deaminase (ADA) in the liver of HUA mice. In the figure, ns represents no significant difference, * represents P < 0.05, ** represents P < 0.01, and **** represents P < 0.0001.

[0055] Figure 4 These are the results of the regulation of A21243 on oxidative stress disorder in HUA mice. In the figure, ns represents no significant difference, * represents P < 0.05, ** represents P < 0.01, *** represents P < 0.001, and **** represents P < 0.0001.

[0056] Figure 5 The figure shows the promoting effect of A21243 on intestinal uric acid excretion in HUA model mice. In the figure, ns represents no significant difference, and ** represents P < 0.01.

[0057] Figure 6 The results show the effect of A21243 on the reduction of renal function indicators creatinine Cr and urea nitrogen BUN and the recovery of renal coefficient in HUA mice. In the figure, ** represents P < 0.01, *** represents P < 0.001, and **** represents P < 0.0001.

[0058] Figure 7 This is the improvement effect of A21243 on the pathological changes in the kidneys and liver of HUA mice.

[0059] Figure 8 The figure shows the effect of A21243 on fasting blood glucose, glycosylated serum protein GSP, and renal function indexes creatinine Cre and urea nitrogen BUN in DKD mice. In the figure, * represents P < 0.05, ** represents P < 0.01, *** represents P < 0.001, and **** represents P < 0.0001.

[0060] Fig. 9 This is the improvement effect of A21243 on renal pathological changes in HUA mice.

[0061] Fig.10 The figure shows the effect of A21243 on serum creatinine and urine creatinine in CKD mice. In the figure, ** represents P < 0.01, and *** represents P < 0.001.

[0062] Fig.11 This is the improvement effect of A21243 on renal pathological changes in CKD mice. DETAILED DESCRIPTION

[0063] The present invention is further described in detail below through specific examples.

[0064] It should be understood that these embodiments are only used to illustrate the present invention and are not used to limit the scope of the present invention.

[0065] In order to make the purpose, technical scheme and advantages of the embodiments of the present invention clearer, the technical scheme in the embodiments of the present invention will be described clearly and completely below. If the specific conditions are not specified in the embodiments, they are carried out according to conventional conditions or conditions recommended by the manufacturer. If the manufacturer of the reagents or instruments used is not specified, they are all conventional products that can be purchased commercially.

[0066] The features and performance of the present invention are further described in detail below in conjunction with the embodiments.

[0067] Example 1 In vitro uric acid-lowering effect of Pediococcus pentosaceus A21243

[0068] Pediococcus pentosaceus A21243 (the deposit number of the bacterium is GDMCCNO:63749, which has been disclosed in the invention patent "A Pediococcus pentosaceus strain A21243 with the function of treating non-alcoholic fatty liver and / or reducing fat and its application, publication number: CN117625478A") was inoculated with an inoculum of 1% in MRS liquid culture medium containing 10 mM uric acid, and cultured anaerobically at 37°C for 24 h. The uric acid content in the culture medium was determined by HPLC, and the same culture medium without inoculation of Pediococcus pentosaceus A21243 was set as a control. The uric acid content was analyzed by HPLC using Agilent Zobax SB-Aq (4.6 mm×250 mm, 5 μm) at 30°C, with a detection wavelength of 293 nm and a mobile phase of 20 mM pH 5. 7.4 K2HPO4-KH2PO4 buffer and methanol (volume ratio of 90:10), flow rate 0.5mL / min, analysis time 15min.

[0069] The in vitro degradation rate of uric acid by Pediococcus pentosaceus A21243 is shown in Table 1, indicating that Pediococcus pentosaceus A21243 has the effect of lowering uric acid in vitro.

[0070] Table 1 Degradation of uric acid by A21243 under nutrient-rich conditions

[0071]

[0072] Example 2 Preparation of a lyophilized powder having the effect of lowering uric acid in a hyperuricemia model

[0073] The freeze-dried powder preparation method of this embodiment comprises the following steps:

[0074] Prepare protective agent: sterilize 12% (W / V) skim milk and 12% (W / V) trehalose at 115°C for 15 min, cool and set aside. When using, mix 12% (W / V) skim milk and 12% (W / V) trehalose in a volume ratio of 1:1.

[0075] Activation and culture of strains: Use an inoculation loop to streak Pediococcus pentosaceus A21243 onto an MRS plate, and culture it under anaerobic conditions at 37°C for 24 hours. Streak the activated single colony again, take the single colony streaked twice and inoculate it into MRS liquid culture medium, and culture it under anaerobic conditions at 37°C for 18 hours. Pick a single colony to 10mL of MRS liquid culture medium, and culture it under anaerobic conditions at 37°C for 12 hours to obtain seed solution 1. Inoculate seed solution 1 into 150mL of MRS liquid culture medium at an inoculation rate of 3%, and culture it under anaerobic conditions at 37°C for 20-22 hours to obtain seed solution 2. Inoculate seed solution 2 into 300mL of MRS liquid culture medium at an inoculation rate of 3%, and culture it under anaerobic conditions at 37°C for 20-24 hours to obtain the bacterial solution after amplification culture. Collect the bacterial solution and centrifuge it in a refrigerated centrifuge at 4°C, 5000rpm, centrifuge for 5 minutes, and discard the supernatant. The bacteria were washed twice with physiological saline, centrifuged at 4°C, 5000 rpm for 5 min, and the wet weight of the bacteria was weighed.

[0076] Vacuum freeze drying: resuspend the lyophilized protective agent and the wet weight of the bacteria at a volume ratio of 1:1 (W:V), divide into EP tubes, and place them at -80℃ for precooling for 1h. Put the divided EP tubes into freeze-dried bottles, freeze-dry the freeze-dried bottles using a four-ring Foring vacuum freeze dryer to freeze-dry the samples, insert the material bottle into the T-shaped frame of the vacuum freeze dryer, unscrew the switch to connect the ampoule tube and the vacuum machine, dry the bacterial agent, and continue freeze drying for 18h to finally obtain a freeze-dried powder containing Pediococcus pentosaceus A21243. Store the finished product in a dry place for later use, and randomly extract part of the freeze-dried powder to prepare a bacterial suspension for specific amplification verification and live bacteria counting.

[0077] Example 3 Uric acid-lowering effect of Pediococcus pentosaceus A21243 on hyperuricemia model mice

[0078] This example is used to investigate the uric acid-lowering effect of Pediococcus pentosaceus A21243 on hyperuricemia (HUA) model mice. The animal experiment steps are as follows:

[0079] 48 SPF-grade C57BL / 6 mice were purchased, male, 6-8 weeks old, weighing 1820 g. Before the experiment, the mice were adaptively raised for 7 days, during which a 12-h light cycle, a temperature of 20-26°C, and a humidity of 40%-60% were maintained. The mice were free to eat and drink. After the adaptation period, they were randomly divided into 4 groups: a normal control group (Control), a hyperuricemia model group (Model), a high-dose group of Pediococcus pentosaceus (A21243 H), and a low-dose group of Pediococcus pentosaceus (A21243L), with 12 mice in each group. The specific grouping operation is as follows:

[0080] Normal control group (Control): fed with basic feed, 0.2 mL of normal saline was intragastrically administered and 0.1 mL of normal saline was intraperitoneally injected for 14 days during the modeling period. After the modeling period, treatment was carried out, and 0.2 mL of normal saline was intragastrically administered and 0.1 mL of normal saline was intraperitoneally injected for 28 days during the treatment period.

[0081] Hyperuricemia model group (Model): During the modeling period, the mice were fed with a high-purine diet containing 28.5% yeast powder, and 250 mg / kg ethambutol hydrochloride was gavaged and 350 mg / kg potassium oxonate was intraperitoneally injected for 14 days. After the modeling period, they entered the treatment period, during which the hyperuricemia model was maintained with a high-purine diet and 350 mg / kg potassium oxonate working solution was intraperitoneally injected for 28 days;

[0082] High-dose group of Pediococcus pentosaceus (A21243 H): During the modeling period, the mice were fed with a high-purine diet containing 28.5% yeast powder, and 250 mg / kg ethambutol hydrochloride was gavaged and 350 mg / kg potassium oxonate was intraperitoneally injected for 14 days. After the modeling period, treatment was carried out. During the treatment period, the hyperuricemia model was maintained with a high-purine diet and 350 mg / kg potassium oxonate was intraperitoneally injected. During the treatment period, high-dose probiotics (i.e., 2×10 9 CFU Pediococcus pentosaceus A21243) were administered intragastrically for 28 days;

[0083] Low-dose group of Pediococcus pentosaceus (A21243 L: During the modeling period, the mice were fed with a high-purine diet containing 28.5% yeast powder, and 250 mg / kg ethambutol hydrochloride was gavaged and 350 mg / kg potassium oxonate was intraperitoneally injected for 14 days. After the modeling period, treatment was carried out. During the treatment period, the hyperuricemia model was maintained with a high-purine diet and 350 mg / kg potassium oxonate was intraperitoneally injected for 28 days. Low-dose probiotics (1×10 8 CFU Pediococcus pentosaceus A21243) were administered intragastrically for 28 days;

[0084] After the modeling period, blood was collected from the orbits of all groups, and the mice were fasted for 12 hours before blood collection. The collected blood was centrifuged at 3500r / min for 15 minutes, and the supernatant (serum) was stored in a -80℃ refrigerator for later use. The supernatant (serum) was taken and the uric acid content was measured using the uric acid detection kit of Nanjing Jiancheng Bioengineering Institute.

[0085] During the modeling period (14 days), the blood uric acid level of each mouse in each group was measured and the mean and standard deviation of the blood uric acid level of each group of mice were calculated. Figure 1 As shown in the figure, there were significant differences between the model group and each strain intervention group and the normal group, and the blood uric acid in each group was 2.0 times higher than that in the normal group. Compared with the model group, there were no significant differences in the Pediococcus pentosaceus A21243 H group and the Pediococcus pentosaceus A21243L group (P>0.05), indicating that the hyperuricemia model was successfully established.

[0086] Intervention period (28 days) and inter-group comparison: After the model was successfully established, the intervention period began. At 2.5 weeks of treatment (18th day of treatment), the blood of mice in the high-dose group of Pediococcus pentosaceus (A21243 H) and the low-dose group of Pediococcus pentosaceus (A21243 L) was collected by orbital bleeding, and the mice were fasted for 12 hours before blood collection. The collected blood was centrifuged at 3500rmp for 15min, and the supernatant (serum) was taken to measure the uric acid content using the uric acid detection kit of Nanjing Jiancheng Bioengineering Institute. At the end of the treatment period (4 weeks, 28th day of treatment), blood was collected from all mice. The collected blood was centrifuged at 3500rmp for 15min, and the supernatant (serum) was taken and stored in a -80℃ refrigerator for standby use, and measured as soon as possible.

[0087] Comparison of uric acid levels among the groups Figure 1 After treatment for 28 days, the serum uric acid level of the model group was significantly increased compared with that of the normal group (P < 0.001), and the serum uric acid level of the high-dose group (A21243 H) and low-dose group (A21243 L) of Pediococcus pentosaceus was significantly reduced compared with that of the model group (P < 0.001), indicating that Pediococcus pentosaceus A21243 has the ability to reduce serum uric acid in hyperuricemia model mice, and there is a certain dose dependence.

[0088] Comparison of uric acid levels in mice before and after the intervention process: At the same time, the changes in uric acid levels of each mouse in each group were compared before and after. The results are as follows: Figure 2As shown. There was no significant difference in blood uric acid between the normal group (Control) and the model group (Model) mice before and after treatment. The blood uric acid of the mice in the high-dose group was significantly reduced after 28 days of intervention (Paired T test, P < 0.001), and the blood uric acid of the mice in the low-dose group was significantly reduced after 18 and 28 days of intervention (Paired T test, P < 0.05). From the significance of the two periods, as the intervention time prolonged, the difference in uric acid between the Pediococcus pentosaceus group and the model group became more significant. Example 4 Inhibitory effect of Pediococcus pentosaceus A21243 on xanthine oxidase (XOD), purine nucleoside phosphorylase (PNP) and adenosine deaminase (ADA) in mouse liver

[0089] This example is used to investigate the inhibitory effect of Pediococcus pentosaceus A21243 on xanthine oxidase (XOD), purine nucleoside phosphorylase (PNP) and adenosine deaminase (ADA) in the liver of HUA model mice. The specific process is as follows:

[0090] Preparation of liver homogenate supernatant: Based on Example 3, each group of mice was euthanized after treatment and dissected. The mouse liver was added with 9 times the volume of 0.9% saline at a ratio of weight (g): volume (mL) = 1:9. The liver was mechanically homogenized under ice water bath conditions to prepare a 10% homogenate at 3000rpm for 10min. The supernatant was divided and frozen at -80°C. It was taken out when needed to avoid repeated freezing and thawing. The assay was performed according to the XOD (Cat. No.: A002-1-1) and ADA (Cat. No.: A048-2-1) detection kits of Nanjing Jiancheng Bioengineering Institute and the PNP detection kit instructions of Shanghai ELISA Biotechnology Co., Ltd.

[0091] The liver XOD values ​​of each group of mice were measured. Figure 3 As shown in the figure, compared with the normal group, the XOD activity of the model mice increased (P < 0.05), and after the intervention of the Pediococcus pentosaceus group A21243 H, the XOD of HUA mice was significantly reduced (P < 0.001). This shows that Pediococcus pentosaceus A21243 has the effect of inhibiting the XOD activity in the liver of hyperuricemia model mice.

[0092] The PNP and ADA values ​​of the livers of mice in each group were measured. Figure 3 As shown, after intervention with Pediococcus pentosaceus group A21243, the activities of PNP and ADA decreased significantly (P < 0.05, P < 0.01).

[0093] XOD, PNP, and ADA are three key enzymes involved in the purine nucleoside decomposition pathway, and the metabolites of the three enzymes are uric acid (UA). The inhibition of XOD, PNP, and ADA activities will lead to the inhibition of uric acid biosynthesis. After the intervention of Pediococcus pentosaceus A21243, the activities of XOD, PNP, and ADA in the liver were inhibited, indicating that it can inhibit the production of uric acid (UA).

[0094] Example 5 Regulatory effect of Pediococcus pentosaceus A21243 on oxidative stress disorder in HUA model mice

[0095] This example is used to investigate the regulatory effect of Pediococcus pentosaceus A21243 on oxidative stress disorders in HUA model mice, including the determination of SOD (superoxide dismutase), CAT (catalase), GSH (glutathione peroxidase) and MDA (malondialdehyde) in mouse liver. The specific process is as follows:

[0096] Weigh the liver of each group of mice (each group of mice treated for 28 days in Example 3), add physiological saline according to the weight ratio of 1:9, use a tissue grinder at 60Hz, run for 10s and stop for 10s, grind for 120s, centrifuge at 4°C, 10000rpm for 10min, take the supernatant and pack it, store it at -80°C, take it out when needed, and avoid repeated freezing and thawing. SOD, CAT, GSH and MDA were measured according to the instructions of the SOD (Cat. No.: A001-3-2), CAT (Cat. No.: A007-1-1), GSH (Cat. No.: A006-2-1) and MDA (Cat. No.: A003-1-2) detection kits of Nanjing Jiancheng Bioengineering Institute.

[0097] The results are as follows Figure 4 As shown. Compared with the normal group, the MDA in the model group increased significantly (P < 0.05), SOD increased significantly (P < 0.05), and CAT increased significantly (P < 0.01). After the intervention of Pediococcus pentosaceus A21243, the MDA in the model group decreased significantly (P < 0.001), SOD and CAT decreased significantly (P < 0.01, P < 0.001), and GSH increased significantly (P < 0.001). After the intervention, MDA, SOD and CAT approached normal, indicating that Pediococcus pentosaceus A21243 can regulate the oxidative stress disorder caused by increased uric acid.

[0098] Example 6 The promoting effect of Pediococcus pentosaceus A21243 on intestinal uric acid excretion in HUA model mice

[0099] This example is used to investigate the promoting effect of Pediococcus pentosaceus A21243 on intestinal uric acid excretion in HUA model mice, and the specific process is as follows:

[0100] After the experiment of Example 3 was completed, the feces of all mice were collected. The feces collected from all mice were added to 9 volumes of 20mmol / L pH 7.4 phosphate buffer at a ratio of weight (g): volume (mL) = 1:9, mechanically homogenized, prepared into a 10% homogenate, 3000 rpm, centrifuged for 10min, and the supernatant was taken for determination using HPLC. HPLC determination was performed using Agilent Zobax SB-Aq (4.6mm×250mm, 5μm) at 30°C to analyze the uric acid content, the detection wavelength was 285nm, the mobile phase was 20mM pH 7.4 K2HPO4-KH2PO4 buffer and methanol (volume ratio of 90:10), the flow rate was 0.5mL / min, and the analysis time was 15min.

[0101] The quantitative analysis results of uric acid in mouse feces are as follows Figure 5 As shown. Compared with the model group, there was no significant difference in the normal control group. After the intervention of Pediococcus pentosaceus A21243, the fecal uric acid was significantly higher than that of the model group (P < 0.01). This shows that after the intervention of Pediococcus pentosaceus A21243H, the excretion of uric acid through feces was promoted, indicating that Pediococcus pentosaceus A21243 has a promoting effect on the excretion of uric acid in the intestine of HUA model mice.

[0102] Example 7 Effect of Pediococcus pentosaceus A21243 on the improvement of renal function indexes in HUA model mice

[0103] This example is used to investigate the improvement effect of Pediococcus pentosaceus A21243 on renal function indicators in HUA model mice, and the specific process is as follows:

[0104] On the 18th and 28th days as in Example 3, the serum of the mice was taken and measured according to the instructions of the detection kits of creatinine (Cre) (Cat. No.: C011-2-1) and urea nitrogen (BUN) (Cat. No.: C013-2-1) of Nanjing Jiancheng Bioengineering Institute. At the same time, when the mice in each group were euthanized and sampled, the weight and kidneys of the mice were weighed, and the kidney coefficient (ratio of kidney to body weight) was calculated.

[0105] The results of the test are as follows Figure 6 As shown in the figure, compared with the normal group, the serum creatinine Cre in the HUA model group was significantly increased (P < 0.01), and the blood urea nitrogen BUN was significantly increased (P < 0.001). Cre and BUN are important indicators for evaluating renal function, indicating that HUA model mice have renal insufficiency, and after the intervention of Pediococcus pentosaceus A21243, serum Cre and BUN were significantly reduced (P < 0.01).

[0106] By calculating the renal coefficient of each group of mice, the results showed that the renal coefficient of the HUA model group was significantly lower than that of the normal group, indicating that the kidney may have atrophy or other degenerative changes. After the intervention of Pediococcus pentosaceus A21243, the renal coefficient returned to normal ( Figure 6 ), indicating that A21243 can improve renal insufficiency caused by hyperuricemia.

[0107] Example 8 Improvement of kidney and liver pathological changes in HUA model mice by Pediococcus pentosaceus A21243

[0108] This example is used to investigate the improvement of Pediococcus pentosaceus A21243 on the pathological changes in the kidney and liver of HUA model mice. The specific process is as follows:

[0109] After the experiment in Example 3, each group of mice was euthanized and samples were collected. 4% paraformaldehyde was used to fix the kidney and liver tissue samples of each group of mice. After dehydration with 50%, 70%, 80%, 90%, 95% and anhydrous ethanol, paraffin was used for embedding, sliced ​​using a microtome, and the paraffin slices were placed in a transparent agent and different concentrations of ethanol in turn to remove the paraffin in the tissue. The slices were placed in a hematoxylin stain for 3 to 8 minutes, then rinsed with tap water, and differentiated with 1% hydrochloric acid alcohol to remove excess hematoxylin dye. 0.6% ammonia water was used for blueing to restore the blue color of the cell nucleus. The slices were placed in an eosin stain for 1 to 3 minutes, and then dehydrated and transparentized with different concentrations of ethanol and xylene in turn. Finally, the slices were sealed with neutral gum for easy microscopic observation.

[0110] The results are as follows Figure 7 As shown, compared with the normal group, ethambutol hydrochloride was used to construct hyperuricemia with renal excretion disorder; compared with the normal group, the model group showed interstitial cell infiltration (red arrow), tubular degeneration (green arrow), glomerular hypertrophy and other conditions in the kidney; and the intervention of Pediococcus pentosaceus A21243 reduced the area of ​​renal pathological changes and the corresponding degree of pathological changes; at the same time, the model group showed mild heparin disorder, hepatocyte swelling (orange-yellow arrow) and mild infiltration of mild inflammatory cells (red arrow) in the liver, and the intervention of Pediococcus pentosaceus A21243 reduced the pathological changes in the liver.

[0111] Example 9 Delay and improvement of renal insufficiency in diabetic nephropathy (DKD) by Pediococcus pentosaceus A21243

[0112] This example is used to investigate the delay and improvement effect of Pediococcus pentosaceus A21243 on diabetic nephropathy (DKD) renal insufficiency, and the specific process is as follows:

[0113] Thirty 6-week-old male C57BL / 6 mice were purchased and fed with a 7-day adaptation period. They were randomly divided into a normal group, a model group, and an A21243 group according to their body weight. The model group and the A21243 group were fed with high-fat and high-fructose (synergistic biological: XTHF60-1) for 14 days, and the A21243 strain was used for preventive intervention at the same time. 0.2 mL 1×10 9 The rats in the control group were injected with streptozotocin (STZ) intraperitoneally on the 14th and 17th days, respectively, with the first dose being 84 mg / kg and the second dose being 65 mg / kg, and the normal group was injected with citric acid buffer intraperitoneally to establish a type 2 diabetes mellitus (T2DM) model.

[0114] Roche blood glucose tester and blood glucose test strips were used to measure the fasting blood glucose of the tail vein blood of each group of mice and the changes in blood glucose after drinking sugar for 2 hours. The fasting blood glucose concentration was greater than 7.0mmol / L, and the blood glucose after drinking sugar for 2 hours was greater than 11.0mmol / L, which was considered a successful model. From the perspective of the mouse state, compared with the normal group, the hair of the model group mice was loose, wet and sticky, and the mice had more urine. The state of A21243 in the intervention group of Pediococcus pentosaceus was relatively good.

[0115] After the model was successfully established, the mice were gavaged with Pediococcus pentosaceus for 28 days. The fasting blood glucose of the mice was measured before the end of the experiment, and a glucose tolerance test (OGTT) was performed. After the intervention, the mice were subjected to cardiac blood sampling and tissue sampling, and mouse serum, kidney and other tissues were collected. Mouse glycosylated serum protein (GSP) (Nanjing Jiancheng kit, item number: A037-2-1), serum creatinine Cr, and urea nitrogen BUN were detected, wherein the detection methods of serum creatinine Cr and urea nitrogen BUN were the same as those in Example 7.

[0116] The results are as follows Figure 8 As shown. The fasting blood glucose in the model group was significantly higher than that in the normal group (P < 0.0001), and the blood glucose value was greater than 11mmol / L, and the glycosylated serum protein in the model group was significantly higher than that in the normal group (P < 0.0001), indicating that the type 2 diabetes model was successfully established. The creatinine and urea nitrogen in the model group were also significantly higher than those in the normal group (P < 0.01, P < 0.05). After the intervention of Pediococcus pentosaceus A21243, the fasting blood glucose and glycosylated serum protein of the model mice were significantly reduced (P < 0.001, P < 0.05), the sugar metabolism capacity was improved, and the renal function indicators creatinine and urea nitrogen were significantly reduced (P < 0.0001, P < 0.01), indicating that Pediococcus pentosaceus A21243 can improve the renal insufficiency caused by type 2 diabetes.

[0117] The mouse kidney was fixed, dehydrated, embedded, sliced, and HE and Masson staining and observed. The specific experimental process was the same as in Example 8, wherein Masson staining was performed according to the instructions of the Masson tricolor staining kit provided by Beyotime Biotech.

[0118] The results are as follows Fig. 9 Compared with the normal group, the diabetic nephropathy model showed interstitial cell infiltration (red arrow), glomerular hypertrophy (red arrow), granulocyte infiltration (green arrow), thickening of glomerular capillary basement membrane and mild mesangial hyperplasia (the collagen of the basement membrane and mesangium was stained bright green, orange-yellow arrow), and after the intervention of Pediococcus pentosaceus A21243, the corresponding pathological changes of the kidneys were alleviated and improved.

[0119] Example 10 Delay and improvement of renal insufficiency caused by cisplatin by Pediococcus pentosaceus A21243

[0120] This example is used to investigate the delay and improvement effect of Pediococcus pentosaceus A21243 on the transformation of acute kidney injury to chronic kidney disease caused by cisplatin, and the specific process is as follows:

[0121] Ten 8-week-old male C57BL / 6 mice were purchased and fed with a basic mouse diet for 7 days. After the adaptation period, they were randomly divided into a normal group, a model group, and an A21243 group according to their body weight. The A21243-containing bacterial powder in Example 2 was used for intervention for 14 days, with an intragastric dose of 1×10 9 CFU, the strain was colonized first, and the normal group and the model group were gavaged with normal saline. The model group and the A21243 group were intraperitoneally injected with cisplatin on the 14th, 21st, and 28th days, respectively, with each dose of 7.5 mg / kg. At the same time, the A21243 group was gavaged with 1×10 9 CFU A21243, normal group and model group were gavaged with normal saline. After the intervention, the animals were euthanized and blood was collected from the heart to measure serum, uric acid Cre and serum BUN. The measurement method was carried out according to the description in the previous example.

[0122] The results are as follows Fig.10 As shown in the figure, serum creatinine in the model group increased significantly compared with the normal group (P < 0.0001), and after the intervention of strain A21243, serum creatinine in the model group decreased significantly (P < 0.01). There was no significant difference in urine protein, but the urine creatinine content in the model group increased significantly. Combined with the results of serum creatinine, more creatinine was accumulated in the model mice, indicating that the renal creatinine excretion capacity decreased, and the model group had renal damage. A21243 intervention can improve renal insufficiency caused by cisplatin.

[0123] At the same time, the kidneys were fixed, dehydrated, embedded, sliced, stained and observed according to the methods in the above examples. Fig.11 As shown in Figure 2, since cisplatin is mainly excreted through the renal tubules and may be reabsorbed and accumulated in the renal tubules, changes in renal tubular morphology such as tubular nephritis are most common, e.g. Fig.11 As shown by the red arrows in the middle, there are a large number of inflammatory cells near the renal tubules. In addition, the renal tubular epithelial cells undergo vacuolar degeneration (green arrows). A21243 intervention alleviated the above pathological changes.

[0124] Embodiment 11

[0125] A solid beverage containing probiotics with uric acid lowering function, comprising, by mass percentage, 40% whole milk powder, 10% oligofructose, 10% trehalose, 10% freeze-dried powder of Pediococcus pentosaceus A21243 strain of Example 2, 10% whey protein powder, 5% citric acid, 5% maltodextrin, 5% carrageenan, and 5% edible flavor.

[0126] The preparation method of the solid beverage comprises the following steps: mixing the ingredients in the above proportions, stirring with a blender for 20 minutes, and then packaging and sealing the mixture with a powder packaging machine to obtain a solid beverage containing probiotics with uric acid-lowering function.

[0127] Example 12

[0128] A microcapsule containing probiotics with uric acid lowering function, comprising a core material, a wall material solution and a cross-linking agent;

[0129] The core material includes Pediococcus pentosaceus A21243, and is prepared by the following method: Pediococcus pentosaceus A21243 is planted in an MRS liquid culture medium, and statically cultured under anaerobic conditions at 37°C for 20 to 24 hours to obtain a cultured bacterial liquid, and the bacterial bodies are collected by centrifugation and washed twice with physiological saline, and centrifuged to obtain the bacterial bodies, that is, the core material is obtained;

[0130] The wall material comprises sodium alginate and modified starch, and is prepared by the following method: a 2% sodium alginate aqueous solution and a 2% modified starch aqueous solution are sterilized and then mixed evenly in a volume ratio of 1:1 to obtain the wall material;

[0131] The cross-linking agent is calcium chloride;

[0132] The preparation method of the above-mentioned microcapsules includes the following steps: mixing the wall material and the core material, spraying them into a crosslinking agent calcium chloride (2%, m / V) solution after atomization through a spray nozzle, so that calcium ions and sodium hyaluronate crosslink to form microcapsules, and statically curing for 120 minutes to obtain microcapsules.

[0133] Example 13

[0134] A method for preparing fermented milk containing probiotics with a uric acid lowering function comprises the following steps: taking the freeze-dried powder of the Pediococcus pentosaceus A21243 strain prepared in Example 2, adding it in an amount of 1% (m / V) to 10 mL of pure cow's milk that has been prepared, homogenized and sterilized, fermenting it at 40°C for 24 hours, adding the obtained fermented liquid as a seed liquid to new pure cow's milk in an amount of 2%, fermenting it at 40°C for 24 hours, and refrigerating it at 4°C for 24 hours to obtain a fermented milk containing probiotics with a uric acid lowering function.

[0135] The viable bacteria count of the fermented milk was greater than 1.0×10 9 CFU / mL.

[0136] Embodiment 14

[0137] A method for preparing a lactic acid bacteria beverage containing probiotics having a uric acid-lowering function, comprising the following steps:

[0138] The freeze-dried powder of Pediococcus pentosaceus A21243 prepared in Example 2 was inoculated at a 5% inoculum into a sterile mixed solution containing 100 L of soy milk, 2 kg of cheese whey and 8 kg of sucrose. After culturing at 40° C. for 20 h, the mixture was filled into beverage bottles using an aseptic filling method to obtain a lactic acid bacteria beverage.

[0139] After the lactic acid bacteria beverage was placed at room temperature of 5°C for 7 days, it was tested and found to be still in a fluid state, with a lactic acid content of 1.2% and a viable bacterial count of more than 10 9 CFU / mL.

[0140] The embodiments of the present invention are described in detail above in conjunction with the accompanying drawings, but the present invention is not limited to the above embodiments. Various changes can be made within the knowledge of ordinary technicians in the relevant technical field without departing from the purpose of the present invention. In addition, the embodiments of the present invention and the features in the embodiments can be combined with each other without conflict.

Claims

1. Use of Pediococcus pentosaceus A21243 or a product thereof in preparing a product for preventing or treating nephropathy, wherein the deposit number of the Pediococcus pentosaceus A21243 is GDMCC NO: 63749.

2. The use according to claim 1, characterized in that: The kidney diseases include renal insufficiency caused by diabetes, hyperuricemia and cisplatin.

3. The use according to claim 2, characterized in that: The diabetes mellitus includes type 2 diabetes mellitus.

4. Use of Pediococcus pentosaceus A21243 or a product thereof in the preparation of a product for preventing or treating hyperuricemia, wherein the deposit number of the Pediococcus pentosaceus A21243 is GDMCC NO:63749.

5. The use according to claim 4, characterized in that: The drug achieves the purpose of preventing or treating hyperuricemia by reducing the uric acid content in the subject's serum, inhibiting the activity of xanthine oxidase, purine nucleoside phosphorylase and / or adenosine deaminase in the subject's liver, regulating the subject's oxidative stress disorder and promoting the subject's excretion of uric acid.

6. The use according to claim 5, characterized in that: The regulating the oxidative stress disorder of the subject includes regulating the contents of SOD, CAT, GSH and MDA in the liver of the subject.

7. The use according to any one of claims 1 to 6, characterized in that: The product comprises at least one of a probiotic preparation containing Pediococcus pentosaceus A21243, a microcapsule, a solid beverage, fermented milk, and a lactic acid bacteria beverage.

8. The use according to claim 7, characterized in that: The products include food and medicine.

9. The use according to claim 8, characterized in that: The product also includes pharmaceutically acceptable excipients; preferably, the pharmaceutically acceptable excipients include at least one of fillers, disintegrants, diluents, dispersants, excipients, stabilizers, lubricants, binders, wetting agents, flavoring agents, suspending agents, solvents, sustained-release agents, emulsifiers, absorption enhancers, surfactants, preservatives, pigments, flavors and solvents.

10. The use according to claim 7, characterized in that: The bacterial count of Pediococcus pentosaceus A21243 in the product is > 10 7 CFU.

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