Bifidobacterium animalis subsp. Lactis HNU329 with uric acid reducing capacity and application thereof

Abstract

The invention provides an animal bifidobacterium subsp. Lactis HNU329 with uric acid reducing ability and application thereof, the animal bifidobacterium subsp. Lactis HNU329 is preserved in Guangdong Microbiological Culture Collection Center GDMCC, the preservation address is Institute of Microbiology, Guangdong Academy of Sciences, on 5th floor, No. 59, No. 100 Courtyard, Xianlie Middle Road, Guangzhou, the preservation date is April 22, 2024, the preservation number is GDMCC No: 64546, and the preservation number is CGMCC No: 64546. The preparation method comprises the following steps of: classifying and naming Bifidobacteria animata subsp.lactis, and carrying out classification and naming on the Bifidobacteria animata subsp.lactis. The strain has good capacity of degrading nucleoside and purine in vitro, also shows good uric acid reducing capacity and anti-inflammatory capacity in animal model evaluation, and can regulate intestinal flora of mice with hyperuricemia and improve symptoms of hyperuricemia. The traditional Chinese medicine composition has no toxic or side effect, high safety and wide application prospect.

Description

Technical Field

[0001] The invention relates to the technical field of hyperuricemia treatment, and relates to a strain of animal Bifidobacterium lactis subspecies HNU329 with uric acid-lowering ability and an application thereof. Background Art

[0002] Hyperuricemia (HUA) is a metabolic disease caused by excessive uric acid production or obstructed uric acid excretion, usually caused by purine metabolism disorders, renal insufficiency or genetic factors. HUA can develop from early benign asymptomatic to more serious chronic gouty arthritis, and may eventually lead to related metabolic diseases such as renal failure, hypertension and atherosclerosis. According to statistics from Coherent Market Insights, the global gout treatment market was valued at US$2.385 billion in 2018, and is expected to grow at a compound annual growth rate of 6.7% during 2019-2027. This will impose a huge medical and economic burden on patients and related health care systems, seriously affecting the economic development of society.

[0003] Currently, the main clinical treatments for HUA are dietary intervention and drug therapy. However, due to the long cycle of dietary intervention and insufficient special nutritional requirements, there are great difficulties in treating HUA. Drug treatment for HUA has the advantages of rapid onset and short course of treatment. However, drug treatment still has great side effects, which can cause allergic reactions and cause varying degrees of damage to the body, and also cause a great economic burden on patients.

[0004] Probiotics are live microorganisms that are beneficial to the host and have a century-long history of promoting human health, especially regulating metabolic disorders. Probiotics are defined as live microorganisms in sufficient numbers that maintain their viability and metabolic activity at all stages of supplement processing. Over the past two decades, probiotics have been recognized as important health promoters due to their diverse properties, and their effects on host metabolism by regulating the intestinal microbiota have been demonstrated in many studies. Probiotics have also made rapid progress in preventing or treating many metabolic diseases, such as type 2 diabetes, obesity, hypertension, and hyperlipidemia.

[0005] At present, the use of probiotics to treat HUA is still in the initial research stage. Some reports show that supplementing with probiotics can reduce the accumulation of uric acid, and can also indirectly reduce uric acid and relieve symptoms of hyperuricemia by regulating intestinal flora and its metabolites. In most scientific studies, the main focus is on the ability of probiotics to reduce nucleosides, and little attention is paid to probiotics that have the ability to reduce both nucleosides and purines. Therefore, screening out probiotics that have the ability to efficiently degrade uric acid precursors and completing the evaluation of the in vivo function of probiotics to relieve HUA will have a theoretical basis and practical significance for the subsequent use of probiotics in the treatment of HUA. Summary of the invention

[0006] In order to overcome the shortcomings of existing research, the purpose of the present invention is to provide a strain of animal Bifidobacterium lactis subspecies HNU329 with the ability to lower uric acid and its application. The strain has the ability to efficiently degrade nucleosides and purines, and has excellent prebiotic properties. It can also effectively reduce serum uric acid levels and alleviate kidney damage in studies on HUA animal models, and has the effect of alleviating and treating HUA.

[0007] The technical solution adopted by the present invention to achieve the technical purpose is:

[0008] The present invention provides a strain of Bifidobacterium animalis subsp. lactis HNU329 with uric acid-lowering ability. The Bifidobacterium animalis subsp. lactis HNU329 has been deposited in the Guangdong Microbial Culture Collection Center (GDMCC), with a deposit address of 5th Floor, Building 59, Compound 100, Xianlie Middle Road, Guangzhou, Institute of Microbiology, Guangdong Academy of Sciences, deposit date of April 22, 2024, deposit number of GDMCC No: 64546, and classification name: Bifidobacterium animalis subsp. lactis.

[0009] Preferably, the Bifidobacterium animalis subsp. lactis HNU329 is capable of degrading inosine, guanosine, guanine, xanthine and hypoxanthine.

[0010] Preferably, the animal Bifidobacterium lactis subspecies HNU329 is acid-resistant and bile-resistant, can survive in a simulated artificial stomach and intestinal fluid environment, and has strong hydrophobicity and self-cohesion.

[0011] The present invention also provides the use of animal Bifidobacterium lactis subspecies HNU329 in the preparation of uric acid-lowering products.

[0012] Preferably, the application includes the application of the Bifidobacterium animalis subspecies lactis HNU329 in the preparation of a product for reducing serum uric acid, urea nitrogen and creatinine levels.

[0013] Preferably, the application includes the application of the Bifidobacterium animalis subsp. lactis HNU329 in the preparation of a product that reduces the activities of xanthine oxidase, adenosine deaminase and purine nucleoside phosphorylase.

[0014] Preferably, the application includes the application of the animal Bifidobacterium lactis subspecies HNU329 in the preparation of a product for reducing the concentration of interleukin 1β (IL-1β), lipopolysaccharide (LPS) and tumor necrosis factor-α (TNF-α) and alleviating inflammatory response.

[0015] Preferably, the application includes the application of the Bifidobacterium animalis subspecies lactis HNU329 in the preparation of a product for alleviating kidney damage and kidney fibrosis caused by hyperuricemia.

[0016] Preferably, the application includes the application of the Bifidobacterium animalis subspecies lactis HNU329 in the preparation of a product for regulating the richness and structure of intestinal flora.

[0017] Preferably, the application includes the application of the Bifidobacterium animalis subspecies lactis HNU329 in the preparation of a product for regulating the composition of intestinal flora.

[0018] The beneficial effects of the present invention are:

[0019] The animal Bifidobacterium lactis subspecies HNU329 screened by the present invention has good ability to degrade nucleosides and purines in vitro, and the strain has excellent tolerance, surface hydrophobicity and self-cohesion. At the same time, it also shows good uric acid-lowering and anti-inflammatory abilities in animal model evaluation, and HNU329 can regulate the intestinal flora of HUA mice after intervention, thereby improving the symptoms of HUA. Compared with traditional drug treatment and dietary control methods, the intervention of probiotic strains has no toxic side effects, high safety, and can prepare corresponding functional uric acid-lowering foods, which is more in line with the needs of modern people in pursuit of healthy life and has broad application prospects. BRIEF DESCRIPTION OF THE DRAWINGS

[0020] Figure 1 HNU329 surface hydrophobicity.

[0021] Figure 2 Effects of HNU329 intervention on serum uric acid, urea nitrogen and creatinine levels in HUA mice.

[0022] Figure 3 Effects of HNU329 intervention on the activities of enzymes related to uric acid metabolism in HUA mice.

[0023] Figure 4 Effect of HNU329 intervention on inflammatory response in HUA mice.

[0024] Figure 5 Effect of HNU329 intervention on renal injury in HUA mice.

[0025] Figure 6 Effects of HNU329 intervention on α-diversity and β-diversity of intestinal flora in HUA mice.

[0026] Figure 7 Effect of HNU329 intervention on the composition of intestinal flora in HUA mice. DETAILED DESCRIPTION

[0027] In order to explain the present invention more clearly, the present invention is further described in detail below in conjunction with embodiments and with reference to the accompanying drawings. It should be understood by those skilled in the art that the content described below is illustrative rather than restrictive, and should not be used to limit the scope of protection of the present invention.

[0028] Example

[0029] 1. Screening of Bifidobacterium animalis subsp. lactis HNU329

[0030] 1. Activation of probiotics and co-cultivation of nucleoside / purine reaction solution

[0031] 53 strains of lactic acid bacteria that were screened and preserved in our laboratory from traditional fermented foods in Hainan, feces of centenarians and healthy infants were activated and inoculated at a 2% inoculation rate into 5 mL of fresh MRS (facultative anaerobic lactic acid bacteria culture medium) / TPY (strict anaerobic culture medium) liquid culture medium and subcultured three times as culture medium.

[0032] 2. Co-culture of probiotic strains with nucleoside / purine reaction solution

[0033] (1) Nucleoside reaction solution and purine reaction solution components

[0034] Nucleoside reaction solution: 1.26mmol / L inosine-1.26mmol / L guanosine-0.1mol / L neutral potassium phosphate solution: Inosine and guanosine reagents are dissolved in 0.1mol / L potassium phosphate solution and fixed to volume with 0.1mol / L potassium phosphate solution (pH 7.0).

[0035] Purine reaction solution: 0.5g / L xanthine-0.5g / L hypoxanthine-0.5g / L guanine-0.1mol / L neutral potassium phosphate solution: xanthine, hypoxanthine and guanine reagents are dissolved in 0.1mol / L potassium phosphate solution and fixed to volume with 0.1mol / L potassium phosphate solution (pH 7.0).

[0036] (2) The activated probiotics were inoculated into 5 mL of MRS (facultative anaerobic lactic acid bacteria medium) / TPY (strict anaerobic medium) medium at a 2% inoculation rate and cultured at 37°C for 24 h. 2 mL of the culture solution was centrifuged at 4°C and 5000 g for 5 min. The cells were suspended in the same volume of physiological saline (85% W / V), washed 3 times and centrifuged to obtain the cells. The cells were then resuspended in 750 μL of nucleoside / purine reaction solution and cultured in a shaking incubator (120 rpm / min, 37°C) for 60 min. After the reaction was completed, the cells were quickly taken out and placed in a boiling water bath for 5 min, the reaction was terminated and cooled to room temperature, centrifuged at 10000 g for 2 min, the supernatant was collected, and the cells were filtered through a 0.22 μm filter for high performance liquid chromatography (HPLC) detection.

[0037] 3. High performance liquid chromatography (HPLC) detection

[0038] (1) Conditions for screening probiotic strains capable of degrading nucleosides:

[0039] Chromatographic column: Agilent ZORBAX SB-Aq chromatographic column (250nm×4.6nm×5μm); flow rate: 1.0mL / min; column temperature: 30℃; mobile phase: methanol and water; detection wavelength 254nm; injection volume 10μL.

[0040] Table 1 Gradient elution program

[0041]

[0042] (2) Conditions for screening probiotic strains capable of degrading purine:

[0043] Chromatographic column: Agilent ZORBAX SB-Aq chromatographic column (250nm×4.6nm×5μm); flow rate: 1.0mL / min; column temperature: 30°C; mobile phase: 0.1% formic acid water+methanol, isocratic elution; detection wavelength 254nm; injection volume 10μL.

[0044] According to the above detection method, the probiotic strains to be tested were screened for uric acid-lowering precursor substances, and the degradation rate of uric acid precursor substances by the strains was as follows:

[0045] Table 2 Standard curves of inosine, guanosine, guanine, xanthine and hypoxanthine

[0046]

[0047] Table 3 Degradation rate of inosine, guanosine, guanine, hypoxanthine and xanthine by lactic acid bacteria

[0048]

[0049]

[0050]

[0051] After screening, a strain of Bifidobacterium animalis lactis subsp. HNU329 was obtained, which has the ability to degrade both nucleosides and purines. As shown in Table 3, its degradation rates for inosine, guanosine, guanine, xanthine and hypoxanthine are 35.71%, 94.28%, 53.15% and 9.86%, respectively.

[0052] Bifidobacterium animalis subsp. lactis HNU329 has been deposited in the Guangdong Microbial Culture Collection Center (GDMCC), the deposit address is: Institute of Microbiology, Guangdong Academy of Sciences, 5th Floor, Building 59, No. 100 Xianlie Middle Road, Guangzhou, Postal Code: 510070, the deposit date is April 22, 2024, the biological deposit number is GDMCC NO: 64546, and the classification name is: Bifidobacteriumanimalis subsp.lactis.

[0053] II. Inhibitory effects of HNU329 intracellular and extracellular metabolites on xanthine oxidase activity

[0054] Extracellular metabolites: The culture solution of the activated strain was centrifuged at 10,000 r / min for 10 min to collect the bacterial precipitate, which was then washed three times with sterile PBS and the concentration of the bacterial suspension was adjusted to 1×10 9 CFU / mL, incubate at 37°C for 12 h, vortex mix, centrifuge the bacterial suspension at 10000 r / min for 10 min, and collect the supernatant.

[0055] Intracellular metabolites: Adjust the concentration to 1×10 9 The bacterial suspension of CFU / mL was broken for 5 min under ultrasonic conditions with a power of 250 W. The obtained liquid was centrifuged at 10000 r / min for 10 min, and the supernatant was collected.

[0056] Xanthine oxidase inhibition rate determination: 50 μL sample and 50 μL xanthine oxidase solution (0.2U) were added to a 96-well plate, shaken for 10 seconds, incubated at 37°C for 5 minutes, and then 150 μL xanthine solution (0.2mM) was added. The absorbance was measured every 30 seconds at 290nm, and the change in absorbance within 10 minutes was recorded. The blank was replaced with 50 μL PBS buffer instead of the sample solution. The xanthine oxidase inhibition activity was calculated according to the following formula:

[0057] Xanthine oxidase inhibition rate (%) = [(d1 / dt)0-(d1 / dt)s] / (d1 / dt)0×100%

[0058] Wherein, (d1 / dt)0: reaction rate of blank; (d1 / dt)s: reaction rate of sample.

[0059] Xanthine oxidase is a key enzyme in purine metabolism that can convert hypoxanthine and xanthine into uric acid and is an important target for the treatment of HUA. The xanthine oxidase inhibition rate was determined (Table 4). The inhibition rates of intracellular metabolites and extracellular metabolites of HNU329 on xanthine oxidase were 17.05% and 58.64%, respectively, indicating that the strain has a certain inhibitory effect on xanthine oxidase activity and can directly reduce the production of uric acid.

[0060] Table 4 Effects of HNU329 intracellular and extracellular metabolites on xanthine oxidase activity

[0061]

[0062] 3. Evaluation of biological characteristics of HNU329

[0063] 1. Acid and bile salt resistance test

[0064] The pH of the liquid culture medium was adjusted to 2, 2.5, and 3 respectively with 0.1 M HCl solution, and a liquid culture medium with a bile salt concentration of 0.3% was prepared and sterilized by high pressure at 121° C. for 15 min.

[0065] The activated HNU329 was inoculated into different pH medium and 0.3% bile salt medium at an inoculum of 2%, and plated after culturing at 37°C for 0, 3 or 4 hours, and the total number of colonies was calculated to set up a control group. The survival rate of the strain (%) = 3h or 4h viable bacteria count / 0h viable bacteria count × 100%.

[0066] 2. Gastrointestinal simulated digestion capacity determination

[0067] Artificial simulated gastric juice (3.5 g / L pepsin, dissolved in sterile PBS, pH = 3.0) and intestinal juice (1.0 g / L trypsin and 0.3% bile salt dissolved in sterile PBS, pH = 6.8) were preheated at 37°C. The bacterial solution was centrifuged at 4000 r / min for 10 min to collect the cells, and the cell concentration was adjusted to 1×10 9 CFU / mL. Take 1mL of bacterial solution and add it to 9mL of simulated gastric fluid and culture it at 37℃ for 0h and 3h, then take samples. Take 1mL of the above culture solution at 3h and add it to 9mL of simulated intestinal fluid. Culture it at 37℃ for 0h and 3h, then take samples and use plate count to determine the total number of viable bacteria. The survival rate of the strain (%) = 3h viable bacteria count / 0h viable bacteria count × 100%.

[0068] Since probiotics must enter the human gastrointestinal tract to exert their probiotic functions, in the process from the mouth to the human intestine, probiotics need to tolerate the low pH environment of the stomach. At the same time, in order for probiotics to reach and colonize in the intestine, they must have a certain tolerance to bile salts. Only strains that can grow and metabolize in normal physiological bile salt mass concentrations can survive in the intestinal digestion process. Therefore, tolerance to acid and bile salts and gastrointestinal simulated digestion ability are important indicators for measuring excellent probiotics. The test results are shown in Table 5. It can be seen that HNU329 not only tolerates low pH environments, with a survival rate of 58.59% under pH = 2 conditions, but also can survive in an environment with a bile salt concentration of 0.3%, and the survival rate after 4 hours still reaches 38.81% (Table 6). HNU329 can also maintain a certain activity after artificial gastric juice and intestinal juice (Table 7).

[0069] Table 5 Survival rate of HUN329 at pH 2.0, pH 2.5 and pH 3.0

[0070]

[0071] Table 6 Survival rate of HNU329 under 0.3% bile salt conditions

[0072]

[0073] Table 7 Number of viable bacteria of HNU329 in simulated gastrointestinal environment

[0074]

[0075] 3. Evaluation of surface hydrophobicity and self-cohesion of HNU329

[0076] (1) Surface hydrophobicity: The activated bacterial solution was centrifuged (4000 g, 10 min) to remove the supernatant, and the bacteria were washed twice with PBS and resuspended in PBS. The concentration of the bacterial suspension was adjusted to 1×10 9 CFU / mL, and measure the absorbance of the bacterial suspension at 600nm (A0). Take the above 3mL bacterial suspension and mix it with 1mL xylene, 1mL hexadecane, 1mL ethyl acetate and 1mL KNO3 respectively, vortex mix for 30s, pause for 10s, and then vortex for 30s. Let it stand at room temperature for 30min to fully stratify, and measure the absorbance of the aqueous phase at 600nm (A1). Repeat the experiment three times and take the average value. The surface hydrophobicity (CSH%) is calculated as follows: surface hydrophobicity (%) = (A0-A1) / A0×100%.

[0077] (2) Self-cohesion: Adjust the concentration of bacterial suspension to 1×10 9CFU / mL, incubate at room temperature for 5 h, and measure the OD value at 600 nm using PBS buffer as a control, which is recorded as At. The experiment was repeated three times and calculated: self-aggregation (%) = 1-At / A0×100%.

[0078] Cell hydrophobicity and self-cohesion are the prerequisites for probiotics to adhere to intestinal epithelial cells and colonize the gastrointestinal tract to exert beneficial effects. Hydrophobicity analysis shows that ( Figure 1 ), HNU329 has strong hydrophobicity, and its hydrophobicity in chloroform (92.50%) is higher than that in xylene (84.53%) and ethyl acetate (23.84%), while the self-cohesion of HNU329 in 5h is 73.76%.

[0079] The results showed that HNU329 exhibited efficient ability to degrade uric acid precursors and excellent prebiotic properties.

[0080] IV. In vivo animal experiments to evaluate the efficacy of HNU329

[0081] 1. Construction of HUA Mouse Model

[0082] Thirty 6-8 week old SFP grade C57BL / 6J mice (20±2g) were selected and randomly divided into a normal group (CON), a model group (MOD) and an HNU329 intervention group (HNU329) after one week of adaptive feeding. All animals were raised under specific pathogen-free conditions and adaptively fed for 7 days. The mice were fed with a laboratory standard diet, free drinking water, and artificial light for 12 hours per day (12 hours of darkness and 12 hours of light alternately). The environmental conditions were controlled at a temperature of 24℃+1℃ and a relative humidity of 55±5%. The modeling and intervention schemes are as follows:

[0083] (1) Normal control group (CON): gavage with 0.5% CMC-Na at 9:00 a.m. every day, followed by gavage with an equal volume of saline 1 hour later for 4 weeks;

[0084] (2) HUA model group (MOD): HUA model was induced by oral gavage of potassium oxonate (250 mg / kg) and inosine (375 mg / kg) and guanosine (375 mg / kg) at 9:00 a.m. every day, and then oral gavage of an equal volume of normal saline was performed 1 hour later for 4 weeks;

[0085] (3) HNU329 intervention group (HNU329): Potassium oxonate (250 mg / kg) and inosine (375 mg / kg) and guanosine (375 mg / kg) were administered orally at 9:00 a.m. every day to induce HUA model. One hour later, 1×10 9 CFU probiotics for 4 weeks. After the intervention period, the mice were euthanized, and the serum, liver, kidney, and intestinal tissues of the mice were collected for relevant measurements.

[0086] 2. Effects of oral administration of HNU329 on HUA mice

[0087] (1) Effect of HNU329 intervention on serum uric acid, urea nitrogen, and creatinine levels in HUA mice: Compared with the model group, HNU329 intervention significantly reduced serum uric acid, urea nitrogen, and creatinine levels in HUA mice ( Figure 2 , p<0.05). Among them, serum uric acid decreased from 107.74μmol / L to 55.47μmol / L, indicating that HNU329 has a significant ability to lower uric acid.

[0088] (2) Effect of HNU329 intervention on the activities of enzymes related to uric acid metabolism in HUA mice: Xanthine oxidase, adenosine deaminase and purine nucleoside phosphorylase are all involved in the body's purine metabolism and are related enzymes that catalyze the production of uric acid. Inhibiting their activity expression can effectively reduce the production of uric acid. The results of the determination of related enzyme activities in the serum and liver of HUA mice showed that compared with the model group, HNU329 intervention reduced the activities of the three uric acid metabolism enzymes by 36.14%, 81.66% and 28.95%, respectively. In particular, HNU329 intervention showed a strong inhibitory effect on the activity of adenosine deaminase, which can effectively alleviate the imbalance of uric acid metabolism ( Figure 3 , p<0.05).

[0089] (3) Effect of HNU329 intervention on inflammatory response in HUA mice: When the uric acid level in the body increases, it will aggravate the oxidative stress effect, release inflammatory mediators, activate inflammatory response, etc., and thus affect the health of the body. Compared with the model group, after HNU329 intervention, the inflammatory response of HUA mice was alleviated, including interleukin 1β (IL-1β), lipopolysaccharide (LPS) and tumor necrosis factor-α (TNF-α), whose concentrations decreased by 13.18%, 27.59% and 21.99%, respectively ( Figure 4 , p<0.05).

[0090] (4) Effect of HNU329 intervention on kidney damage in HUA mice: The kidney is an important site for the removal of uric acid, and hyperuricemia is closely related to kidney damage. The results of kidney H&E and MASSON staining showed that HNU329 intervention could reduce kidney damage and renal fibrosis in HUA mice ( Figure 5 ).

[0091] (5) Effects of HNU329 intervention on α-diversity and β-diversity of intestinal flora in HUA mice: Studies have shown that changes in the structure of intestinal flora may cause uric acid metabolism disorders, which are involved in the synthesis of purine metabolic enzymes and the release of inflammatory factors, and are closely related to the occurrence and development of HUA. Compared with the model group, after HNU329 intervention, the α-diversity of the intestinal flora of HUA mice increased at the genus and species levels, and the changes were significant ( Figure 6 , p<0.05). Similarly, in the principal component analysis (PCA) based on the genus level and species level, the samples of each group were divided into different groups, indicating that the structure of the intestinal flora changed between different groups. And the changes in the intestinal flora community structure of HUA mice treated with HNU329 tended to be similar to that of CON group mice ( Figure 6 , p<0.05). The results showed that HNU329 intervention could regulate the richness and structure of the intestinal flora in HUA mice.

[0092] (6) Effect of HNU329 intervention on the composition of the intestinal flora of HUA mice: Based on the NR species annotation results, after HNU329 intervention, the community composition of the intestinal flora of HUA mice changed at the genus and species levels. At the genus level, Duncaniella, Bacteroides, and Heminiphilus accounted for a large proportion of abundance; at the species level, Bacteroides sp., Duncaniella sp., and Heminiphilus faecis accounted for a large proportion of abundance ( Figure 7 ). The results showed that HNU329 intervention could regulate the composition of intestinal flora in HUA mice and thus affect the occurrence and development of HUA.

[0093] The present invention explores that a strain of animal Bifidobacterium lactis subspecies HNU329 screened out from in vitro experiments has the ability to efficiently degrade nucleosides and purines, and has excellent properties of acid resistance and bile salt resistance, and has a high survival rate in simulated artificial stomach and intestinal fluid environments, and has strong surface hydrophobicity and self-cohesion. In an in vivo animal model, HNU329 intervention has a good effect on relieving hyperuricemia, can reduce serum uric acid levels and inflammatory reactions, slow down kidney damage and regulate intestinal flora, and the strain can be widely used in the production of uric acid-lowering foods, etc.

[0094] Obviously, the above embodiments of the present invention are merely examples to more clearly illustrate the present invention, and are not limitations on the implementation methods of the present invention. For ordinary technicians in the relevant field, other different forms of changes or modifications can be made on the basis of the above description. It is impossible to list all the implementation methods here. All obvious changes or modifications derived from the technical solution of the present invention are still within the protection scope of the present invention.

Claims

1. A strain of Bifidobacterium animalis subsp. lactis HNU329 with the ability to lower uric acid, wherein the Bifidobacterium animalis subsp. lactis HNU329 has been deposited in the Guangdong Provincial Microbial Culture Collection Center GDMCC, the storage address: Institute of Microbiology, Guangdong Academy of Sciences, 5th Floor, Building 59, No. 100 Xianlie Middle Road, Guangzhou, the storage date is April 22, 2024, the storage number is GDMCC No: 64546, and the classification name is: Bifidobacterium animalis subsp. lactis.

2. The animal Bifidobacterium lactis subspecies HNU329 according to claim 1, characterized in that The Bifidobacterium animalis subspecies lactis HNU329 is capable of degrading inosine, guanosine, guanine, xanthine and hypoxanthine.

3. The animal Bifidobacterium lactis subspecies HNU329 according to claim 1, characterized in that The animal Bifidobacterium lactis subspecies HNU329 has the characteristics of acid resistance and bile salt resistance, can survive in a simulated artificial stomach and intestinal fluid environment, and has strong hydrophobicity and self-cohesion.

4. Use of the animal Bifidobacterium lactis subspecies HNU329 according to any one of claims 1 to 3 in the preparation of a product for lowering uric acid.

5. The use according to claim 4, characterized in that: The application includes the application of the animal Bifidobacterium lactis subspecies HNU329 in the preparation of products for reducing serum uric acid, urea nitrogen and creatinine levels.

6. The use according to claim 4, characterized in that: The application includes the application of the animal Bifidobacterium lactis subspecies HNU329 in the preparation of a product for reducing the activities of xanthine oxidase, adenosine deaminase and purine nucleoside phosphorylase.

7. The use according to claim 4, characterized in that: The application includes the application of the animal Bifidobacterium lactis subspecies HNU329 in the preparation of a product for reducing the concentration of interleukin-1β, lipopolysaccharide and tumor necrosis factor-α and alleviating inflammatory response.

8. The use according to claim 4, characterized in that: The application includes the application of the animal Bifidobacterium lactis subspecies HNU329 in the preparation of a product for alleviating kidney damage and kidney fibrosis caused by hyperuricemia.

9. The use according to claim 4, characterized in that: The application includes the application of the animal Bifidobacterium lactis subspecies HNU329 in the preparation of products for regulating the richness and structure of intestinal flora.

10. The use according to claim 4, characterized in that: The application includes the application of the animal Bifidobacterium lactis subspecies HNU329 in the preparation of products for regulating the composition of intestinal flora.

Images