Preventive potential of Lactobacillus johnsonii YH1136 against uric acid accumulation and hyperuricemia- induced damages in rats

Abstract

Abstract Background Hyperuricemia (HUA) is a prevalent metabolic disorder globally, and its development is increasingly associated with intestinal microbiota. Therefore, probiotics have emerged as a potential and safe approach for lowering uric acid (UA) levels. However, effective probiotic strains and the underlying mechanism remain unknown. Purpose This study aims to investigate microbiota alterations in each intestinal segment during HUA to identify the most affected segment and potential probiotic strains. Methods This study contains two animal experiments. In the first animal experiment, male SD rats were randomly divided into two groups and administered with either 0.5%CMC (Control group) or potassium oxonate (Model group) by oral gavage for an 84-days period. After sacrifice, the whole Gut microbiota was analyzed. In the ssecond animal experiment,Male SD rats were randomly divided into three groups with Control and model groups treated the same as former experiment, while YH1136 group was treated by Lactobacillus johnsonii YH1136 instead (daily amounts of 2×108 CFU). Results Whole intestinal diversity was significantly decreased in the model group than in the control, with the most significant decrease in the cecum and colon. Firmicutes, Bacteroidota, and Actinobacteriota were the dominant phyla common to the control and model groups, whereas Bacteroidota was more dominant in the colon of the model group than in the control group. In the RDA analysis, Lactobacillus in the colon and the model group exhibited a strong correlation, suggesting that Lactobacillus may play an important role in hyperuricemia. Consequently, Lactobacillus johnsonii YH1136 was used to assess its preventive effects against HUA. The results showed that Lactobacillus johnsonii YH1136 administration effectively reduced serum UA levels in vivo, mainly inhibiting hepatic xanthine oxidas(XOD) activity and promoting renal ABCG2 transporter expression.Moreover, increased colonization using Lactobacillus johnsonii YH1136 significantly ameliorated pathological damage in the kidney and liver, causing UA accumulation. Conlusion These findings highlight the potential significance of Lactobacillus as a connection between HUA and the gut microbiota, providing compelling evidence for Lactobacillus johnsonii YH1136 as a potential treatment for HUA.