Animal bifidobacterium lactis strain hnu329 with uric acid reducing ability and application thereof

Abstract

The application provides an animal Bifidobacterium lactis HNU329 with the ability of reducing uric acid and an application thereof, the animal Bifidobacterium lactis HNU329 has been preserved in the Guangdong Microbial Culture Collection Center (GDMCC), the preservation address is the 5th floor of the 59th building of the courtyard, No. 100, Jiefang Road, Guangzhou, the preservation date is April 22, 2024, the preservation number is GDMCC No: 64546, and the classification and naming are Bifidobacterium animalis subsp. Lactis. The strain has good degradation abilities of nucleosides and purines in vitro, also shows good uric acid reducing ability and anti-inflammatory ability in animal model evaluation, and can regulate the intestinal flora of hyperuricemia mice and improve the symptoms of hyperuricemia. The strain is non-toxic and has no side effects, is safe, and has a wide application prospect.

Description

Technical Field

[0001] This invention relates to the field of hyperuricemia treatment technology, and to a strain of Bifidobacterium animalis subsp. lactis HNU329 with uric acid-lowering ability and its application. Background Technology

[0002] Hyperuricemia (HUA) is a metabolic disease caused by excessive uric acid production or impaired uric acid excretion, typically resulting from purine metabolism disorders, renal insufficiency, or genetic factors. HUA can progress from early benign, asymptomatic stages to more severe chronic gouty arthritis, ultimately potentially leading to related metabolic diseases such as kidney failure, hypertension, and atherosclerosis. According to Coherent Market Insights, the global gout treatment market was valued at US$2.385 billion in 2018 and is projected to grow at a CAGR of 6.7% from 2019 to 2027. This will impose a significant medical and economic burden on patients and related healthcare systems, severely impacting societal and economic development.

[0003] Currently, the main clinical treatments for hypertrophic angina (HUA) are dietary intervention and drug therapy. However, dietary intervention is time-consuming and often involves insufficient special nutritional needs, making it challenging to treat HUA effectively. Drug therapy for HUA has advantages such as rapid onset of action and short treatment course; however, it still has significant side effects, which can cause severe allergic reactions and varying degrees of damage to the body, while also placing a substantial financial burden on patients.

[0004] Probiotics are live microorganisms that are beneficial to the host and have a history of promoting human health, particularly regulating metabolic disorders, spanning over a century. Probiotics are defined as a sufficient number of live microorganisms 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 influence on host metabolism through the regulation of the gut microbiota has been confirmed in numerous studies. Probiotics have also made rapid progress in the prevention or treatment of many metabolic diseases, such as type 2 diabetes, obesity, hypertension, and hyperlipidemia.

[0005] Currently, the use of probiotics to treat hyperuricemia (HUA) is still in its early research stages. Some reports suggest that probiotic supplementation can reduce uric acid accumulation and indirectly lower uric acid levels by regulating gut microbiota and its metabolites, thus alleviating hyperuricemia symptoms. Most scientific research focuses on the nucleoside-lowering ability of probiotics, with little attention paid to probiotics that simultaneously lower both nucleoside and purine levels. Therefore, screening for probiotics with highly efficient uric acid precursor degradation capabilities and evaluating their in vivo efficacy in alleviating HUA will provide a theoretical basis and practical significance for the subsequent use of probiotics in HUA treatment. Summary of the Invention

[0006] To overcome the shortcomings of existing research, the present invention aims to provide a strain of Bifidobacterium lactis HNU329 with uric acid-lowering ability and its application. This strain has a high efficiency in degrading nucleosides and purines and has excellent probiotic properties. In studies on HUA animal models, it has also been able to effectively reduce serum uric acid levels and alleviate kidney damage, and has the effect of relieving and treating HUA.

[0007] The technical solution adopted by this invention to achieve its technical objectives is as follows:

[0008] This invention provides a strain of Bifidobacterium animalis subsp. lactis HNU329 with uric acid-lowering ability. The strain has been deposited at the Guangdong Provincial Microbial Culture Collection Center (GDMCC), located at the Institute of Microbiology, Guangdong Academy of Sciences, 5th Floor, Building 59, No. 100 Xianlie Middle Road, Guangzhou, on April 22, 2024, with accession number 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 Bifidobacterium lactis subsp. HNU329 has acid and bile salt resistance, can survive in a simulated artificial gastric and intestinal fluid environment, and has strong hydrophobicity and self-cohesion.

[0011] This invention also provides the application of Bifidobacterium animalis subsp. lactis HNU329 in the preparation of products that lower uric acid.

[0012] Preferably, the application includes the use of Bifidobacterium lactis subsp. HNU329 in the preparation of products that reduce serum uric acid, urea nitrogen and creatinine levels.

[0013] Preferably, the application includes the use of Bifidobacterium animalis subspecies HNU329 in the preparation of products that reduce the activity of xanthine oxidase, adenosine deaminase and purine nucleoside phosphorylase.

[0014] Preferably, the application includes the use of Bifidobacterium lactis subsp. HNU329 in the preparation of products that reduce the concentrations of interleukin-1β (IL-1β), lipopolysaccharide (LPS), and tumor necrosis factor-α (TNF-α) and alleviate inflammatory responses.

[0015] Preferably, the application includes the use of Bifidobacterium lactis subspecies HNU329 in the preparation of products that alleviate kidney damage and renal fibrosis caused by hyperuricemia.

[0016] Preferably, the application includes the use of Bifidobacterium animalis subspecies HNU329 in the preparation of products that regulate the richness and structure of the intestinal flora.

[0017] Preferably, the application includes the use of Bifidobacterium animalis subspecies HNU329 in the preparation of products that regulate the composition of the intestinal flora.

[0018] The beneficial effects of this invention are as follows:

[0019] The *Bifidobacterium animalis* subspecies *Lactobacillus* HNU329 screened in this invention exhibits excellent ability to degrade nucleosides and purines in vitro, and demonstrates superior tolerance, surface hydrophobicity, and self-aggregation. Furthermore, it showed good uric acid-lowering and anti-inflammatory capabilities in animal models, and intervention with HNU329 could regulate the gut microbiota of hyperuricemic (HUA) mice, thereby improving HUA symptoms. Compared with traditional drug treatments and dietary control methods, the intervention with probiotic strains has no toxic side effects, high safety, and can be used to prepare corresponding functional uric acid-lowering foods, better meeting the needs of modern people pursuing a healthy lifestyle and possessing broad application prospects. Attached Figure Description

[0020] Figure 1 HNU329 surface hydrophobicity.

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

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

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

[0024] Figure 5 Effects of HNU329 intervention on kidney damage in HUA mice.

[0025] Figure 6 Effects of HNU329 intervention on α and β diversity of gut microbiota in HUA mice.

[0026] Figure 7 Effects of HNU329 intervention on gut microbiota composition in HUA mice. Detailed Implementation

[0027] To more clearly illustrate the present invention, the invention will be further described in detail below with reference to embodiments and accompanying drawings. Those skilled in the art should understand that the specific description below is illustrative rather than restrictive and should not be construed as limiting the scope of protection of the present invention.

[0028] Example

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

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

[0031] Fifty-three strains of lactic acid bacteria, which were previously screened and preserved in our laboratory from traditional fermented foods in Hainan, feces from long-lived elderly people, and feces from healthy infants, were activated and then inoculated into 5 mL of fresh MRS (facultative anaerobic lactic acid bacteria medium) / TPY (strictly anaerobic medium) liquid medium at a 2% inoculation rate. The medium was then subcultured three times to obtain the culture medium.

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

[0033] (1) Components of nucleoside reaction solution and purine reaction solution

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

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

[0036] (2) Activated probiotics were inoculated at a rate of 2% into 5 mL of MRS (facultative anaerobic lactic acid bacteria medium) / TPY (strictly anaerobic medium) and cultured at 37℃ for 24 h. 2 mL of the culture solution was then centrifuged at 5000 g for 5 min at 4℃. The bacterial cells were resuspended in the same volume of physiological saline (85% W / V), washed three times, and centrifuged again to obtain the bacterial cells. The cells were then resuspended in 750 μL of nucleoside / purine reaction solution and cultured in a shaking incubator (120 rpm / min, 37℃) for 60 min. After the reaction was complete, the cells were immediately removed and placed in a boiling water bath for 5 min to terminate the reaction. The cells were then cooled to room temperature and centrifuged at 10000 g for 2 min. The supernatant was collected and filtered through a 0.22 μm filter membrane for high-performance liquid chromatography (HPLC) detection.

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

[0038] (1) Conditions for screening probiotic strains with nucleoside degradation capabilities:

[0039] Chromatographic column: Agilent ZORBAX SB-Aq 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 with purine-degrading ability:

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

[0044] Following the above detection method, the probiotic strains to be tested were screened for uric acid-lowering precursor substances. The degradation rates of uric acid precursor substances by the strains are as follows:

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

[0046]

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

[0048]

[0049]

[0050]

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

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

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

[0054] Extracellular metabolites: The activated bacterial culture medium was centrifuged at 10,000 r / min for 10 min to collect the bacterial pellet. The pellet was washed three times with sterile PBS, and the bacterial suspension concentration was adjusted to 1×10⁻⁶. 9 The bacterial suspension was incubated at 37°C for 12 hours with CFU / mL, then vortexed to mix. The suspension was then centrifuged at 10,000 rpm for 10 minutes, and the supernatant was collected.

[0055] Intracellular metabolites: Adjust the concentration to 1×10 9 The bacterial suspension of CFU / mL was disrupted by sonication at 250W for 5 min. The resulting liquid was centrifuged at 10000 rpm for 10 min, and the supernatant was collected.

[0056] Xanthine oxidase inhibition rate assay: Add 50 μL of sample and 50 μL of xanthine oxidase solution (0.2 U) to each well of a 96-well plate. After shaking for 10 s, incubate at 37°C for 5 min, then add 150 μL of xanthine solution (0.2 mM). Measure the absorbance at 290 nm every 30 s and record the change in absorbance over 10 min. Use 50 μL of PBS buffer instead of the sample solution as a blank. Calculate the xanthine oxidase inhibitory activity using the following formula:

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

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

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

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

[0061]

[0062] III. Evaluation of the biological characteristics of HNU329

[0063] 1. Acid and bile salt resistance tests

[0064] The pH of the liquid culture medium was adjusted to 2, 2.5 and 3 respectively using 0.1M HCl solution, and a liquid culture medium with a concentration of 0.3% bile salts was prepared and autoclaved at 121℃ for 15 min.

[0065] Activated HNU329 was inoculated at a rate of 2% into culture media with different pH values ​​and 0.3% bile salt medium. After incubation at 37°C for 0, 3, or 4 hours, the culture was plated and the total colony count was calculated. A control group was also included. The survival rate (%) of the strain was calculated as: (Number of viable cells at 3 hours or 4 hours) / (Number of viable cells at 0 hours) × 100%.

[0066] 2. Gastrointestinal simulated digestive capacity measurement

[0067] Artificial 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 salts dissolved in sterile PBS, pH 6.8) were preheated at 37°C. The bacterial culture was centrifuged at 4000 rpm for 10 min to collect the cells, and the cell concentration was adjusted to 1 × 10⁻⁶ cells / mL with sterile PBS. 9 CFU / mL. Take 1 mL of bacterial culture and add it to 9 mL of simulated gastric fluid. Incubate at 37°C for 0 h and 3 h, then take samples. At 3 h, take 1 mL of the above culture and add it to 9 mL of simulated intestinal fluid. Incubate at 37°C for 0 h and 3 h, then take samples and determine the total viable count using plate counting. The survival rate (%) of the strain = (3 h viable count / 0 h viable count) × 100%.

[0068] Since probiotics must enter the human gastrointestinal tract to exert their beneficial functions, they need to tolerate the low pH environment of the stomach during the journey from the mouth to the intestines. Simultaneously, for probiotics to reach and colonize the intestines, they must have a certain tolerance to bile salts. Only strains capable of growing and metabolizing in normal physiological bile salt concentrations can survive during intestinal digestion. Therefore, tolerance to acid and bile salts, as well as the ability of the gastrointestinal tract to simulate digestion, are important indicators for evaluating superior probiotics. The test results, as shown in Table 5, indicate that HNU329 not only tolerates low pH environments (58.59% survival rate at pH=2), but also survives in an environment with a 0.3% bile salt concentration, with a survival rate still reaching 38.81% after 4 hours (Table 6). HNU329 also maintains a certain level of activity after exposure to simulated gastric and intestinal fluids (Table 7).

[0069] Table 5. Survival rates 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. Viable bacterial count of HNU329 in a simulated gastrointestinal environment.

[0074]

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

[0076] (1) Surface hydrophobicity: Centrifuge the activated bacterial suspension (4000g, 10min) and discard the supernatant. Wash the bacterial cells twice with PBS, resuspend them in PBS, and adjust the bacterial suspension concentration to 1×10⁻⁶. 9 The absorbance (A0) of the bacterial suspension at 600 nm was measured simultaneously using CFU / mL. 3 mL of the bacterial suspension was mixed with 1 mL xylene, 1 mL n-hexadecane, 1 mL ethyl acetate, and 1 mL KNO3, respectively. The mixture was vortexed for 30 seconds, paused for 10 seconds, and then vortexed again for 30 seconds. The mixture was then allowed to stand at room temperature for 30 minutes to allow for complete separation. The absorbance (A1) of the aqueous phase at 600 nm was measured. The experiment was repeated three times, and the average value was taken. The surface hydrophobicity (CSH%) was calculated using the following formula: Surface hydrophobicity (%) = (A0 - A1) / A0 × 100%.

[0077] (2) Self-coagulation: Adjust the bacterial suspension concentration to 1×10 9The concentration was CFU / mL, and the mixture was incubated at room temperature for 5 hours. The OD value was measured at 600 nm using PBS buffer as a control, and recorded as At. The experiment was repeated three times, and the self-cohesive force (%) was calculated as: 1 - At / A0 × 100%.

[0078] Cellular hydrophobicity and self-cohesion are prerequisites for probiotics to adhere to intestinal epithelial cells, colonize the gastrointestinal tract, and exert beneficial effects. Hydrophobicity analysis shows that ( Figure 1 HNU329 exhibits strong hydrophobicity, with its hydrophobicity in chloroform (92.50%) being higher than that in xylene (84.53%) and ethyl acetate (23.84%). Furthermore, HNU329 maintains a self-cohesive strength of 73.76% after 5 hours.

[0079] The results showed that HNU329 exhibited a high capacity for degrading uric acid precursors and excellent probiotic properties.

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

[0081] 1. Construction of the HUA mouse model

[0082] Thirty 6-8 week old SFP-grade C57BL / 6J mice (20±2g) were selected and, after one week of acclimatization, randomly divided into a normal control group (CON), a model group (MOD), and an HNU329 intervention group (HNU329). All animals were housed under specific pathogen-free conditions for 7 days of acclimatization. Mice were fed a standard laboratory diet, had free access to water, and were exposed to artificial light for 12 hours daily (alternating between 12 hours of darkness and 12 hours of light). Environmental conditions were controlled at a temperature of 24℃±1℃ and a relative humidity of 55±5%. The modeling and intervention protocols are as follows:

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

[0084] (2) HUA model group (MOD): At 9:00 a.m. every day, potassium oxonate (250 mg / kg) and inosine (375 mg / kg) and guanosine (375 mg / kg) were administered by gavage to induce the HUA model. One hour later, an equal volume of physiological saline was administered by gavage. This was continued for 4 weeks.

[0085] (3) HNU329 intervention group (HNU329): At 9:00 AM daily, potassium oxonate (250 mg / kg) and inosine (375 mg / kg) were administered by gavage, and guanosine (375 mg / kg) was administered in combination to induce the HUA model. One hour later, 1×10 9 CFU probiotics were administered for 4 weeks. After the intervention period, the mice were euthanized, and relevant measurements were taken from their serum, liver, kidney, and intestinal tissues.

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

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

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

[0089] (3) Effects of HNU329 intervention on inflammatory response in HUA mice: When uric acid levels rise in the body, oxidative stress is aggravated, inflammatory mediators are released, and inflammatory responses are activated, thus affecting the body's health. Compared with the model group, HNU329 intervention reduced the inflammatory response in HUA mice, including interleukin-1β (IL-1β), lipopolysaccharide (LPS), and tumor necrosis factor-α (TNF-α), with concentrations decreasing by 13.18%, 27.59%, and 21.99%, respectively. Figure 4 (p<0.05).

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

[0091] (5) Effects of HNU329 intervention on gut microbiota α- and β-diversity in HUA mice: Studies have shown that changes in gut microbiota structure 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 gut microbiota in HUA mice increased at both the genus and species levels, and the changes were significant. Figure 6 (p<0.05). Similarly, principal component analysis (PCA) at the genus and species levels showed that the samples were divided into different taxa, indicating changes in the structure of the gut microbiota among different groups. Furthermore, the gut microbiota community structure of HNU329-treated HUA mice tended to resemble that of the CON group mice (…). Figure 6 (p<0.05). The results showed that HNU329 intervention could regulate the richness and structure of the gut microbiota in HUA mice.

[0092] (6) Effects of HNU329 intervention on gut microbiota composition in HUA mice: Based on NR species annotation results, HNU329 intervention altered the community composition of gut microbiota in HUA mice at both the genus and species levels. At the genus level, Duncaniella, Bacteroides, and Heminiphilus had higher abundance ratios; at the species level, Bacteroides sp., Duncaniella sp., and Heminiphilus faecis had higher abundance ratios. Figure 7 The results showed that HNU329 intervention could regulate the composition of the gut microbiota in HUA mice, thereby affecting the occurrence and development of HUA.

[0093] This invention explores the efficient degradation of nucleosides and purines by *Bifidobacterium lactis* subspecies HNU329, screened from in vitro experiments. It exhibits excellent acid and bile salt resistance, high survival rates in simulated gastric and intestinal fluid environments, and strong surface hydrophobicity and self-aggregation. In in vivo animal models, HNU329 intervention showed good effects in alleviating hyperuricemia, reducing serum uric acid levels and inflammatory responses, mitigating kidney damage, and regulating intestinal flora. This strain can be widely used in the production of uric acid-lowering foods.

[0094] Obviously, the above embodiments of the present invention are merely examples to illustrate the present invention more clearly, and are not intended to limit the implementation of the present invention. For those skilled in the art, other variations or modifications can be made based on the above description. It is impossible to exhaustively list all implementation methods here. Any obvious variations or modifications derived from the technical solutions of the present invention are still within the protection scope of the present invention.

Claims

1. A strain of Bifidobacterium animalis subsp. lactis with uric acid-lowering ability ( HNU329, accession number GDMCC No: 64546.

2. The Bifidobacterium lactis subspecies HNU329 according to claim 1, characterized in that, The animal bifidobacterium lactis subspecies HNU329 can degrade inosine, guanosine, guanine, xanthine, and hypoxanthine.

3. The Bifidobacterium lactis subspecies HNU329 according to claim 1, characterized in that, The animal Bifidobacterium lactis subspecies HNU329 has acid and bile salt resistance, can survive in simulated artificial gastric and intestinal fluid environments, and has strong hydrophobicity and self-aggregating ability.

4. The use of Bifidobacterium lactis subsp. HNU329 as described in any one of claims 1 to 3 in the preparation of uric acid-lowering drugs.

5. The application according to claim 4, characterized in that, The applications include the use of Bifidobacterium lactis subsp. HNU329 in the preparation of pharmaceuticals that reduce serum uric acid, urea nitrogen and creatinine levels.

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