Abstract: Objective: To find a novel probiotic strain capable of effectively alleviating hyperuricemia (HUA) and to validate its inhibitory effect on HUA in an animal model. Methods: All mice were randomly divided into four groups (n = 6 per group): control (CON), HUA model, Bacillus paralicheniformis Q13 intervention (Q13), and allopurinol intervention (ADC). The modeling and administration lasted for a total of 14 days. One hour after the final administration, blood, kidney, liver, colon, and feces samples were collected from each group for subsequent analysis. The disc diffusion method was employed to evaluate the susceptibility of this strain to 13 antibiotics and the tolerance to gastric and intestinal fluids was assessed. Results: Q13 effectively alleviated the elevation of serum uric acid levels, inhibited the activity of xanthine oxidase in the liver (P < 0.01), and protected renal function in mice. Furthermore, Q13 significantly increased hepatic superoxide dismutase (SOD) activity (P < 0.01) and decreased hepatic malondialdehyde (MDA) content (P < 0.01) in mice. It helped maintain normal high-density lipoprotein cholesterol (HDL-C) levels while significantly reducing low-density lipoprotein cholesterol (LDL-C) levels (P < 0.05). Q13 also reduced endotoxin levels in the liver (P < 0.01) and inhibited the secretion of renal inflammatory cytokines such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) (P < 0.01), as well as ameliorating the histopathological changes of the kidney, liver, and colon. Moreover, it rectified the dysbiosis of gut microbiota induced by potassium oxonate, restoring the Bacteroidetes-to-Firmicutes ratio (Bac/Firm ratio) to the level of the CON group and decreasing the abundance of the inflammation-associated phylum TM7. Q13 was susceptible or moderately susceptible to all 13 antibiotics. The 4-h survival rate of Q13 was over 95% in artificial gastric juice and over 86% in artificial intestinal juice. Conclusion: B. paralicheniformis Q13 significantly inhibited the elevation of uric acid and enhanced renal function. Moreover, it significantly down-regulated xanthine oxidase activity, mitigated renal, hepatic and colonic injury induced by potassium oxonate in mice, abated renal inflammation, boosted hepatic antioxidant function, and modulated the homeostasis of gut microbiota, ultimately alleviating HUA. This study provides scientific support for the development of probiotic products containing B. paralicheniformis Q13 for preventing and alleviating HUA.

Key words: Bacillus paralicheniformis; hyperuricemia; renal damage; xanthine oxidase; oxidative stress