Probiotic Bacillus Alleviates Oxidative Stress-Induced Liver Injury by Modulating Gut-Liver Axis in a Rat Model

Emerging evidence suggests a key role of gut microbiota in maintaining liver functions through modulating the gut–liver axis. In this study, we investigated whether microbiota alteration mediated by probiotic Bacillus was involved in alleviating oxidative stress- induced liver injury. Sprague–Dawley rats were orally administered Bacillus SC06 or SC08 for a 24-day period and thereafter intraperitoneally injected diquat (DQ) to induce oxidative stress. Results showed that Bacillus, particularly SC06 significantly inhibited hepatic injuries, as evidenced by the alleviated damaged liver structure, the decreased levels of ALT, AST, ALP and LDH, and the suppressed mitochondrial dysfunction. SC06 pretreatment markedly enhanced the liver antioxidant capacity by decreasing MDA and p47, and increasing T-AOC, SOD and HO-1.16S rRNA sequencing analysis revealed that DQ significantly changed the diversities and composition of gut microbiota, whereas Bacillus pretreatments could attenuate gut dysbiosis. Pearson’s correlation analysis showed that AST and MDA exerted a positive correlation with the opportunistic pathogenic genera and species (Escherichia and Shigella), and negatively correlated with the potential probiotics (Lactobacillus), while SOD exerted a reverse trend. The microbial metagenomic analysis demonstrated that Bacillus, particularly SC06 markedly suppress the metabolic pathways such as carbohydrate metabolism, lipid metabolism, amino acid metabolism and metabolism of cofactors and vitamins. Furthermore, SC06 decreased the gene abundance of the pathways mediating bacterial replication, secretion and pathogenicity. Taken together, Bacillus SC06 alleviates oxidative stress-induced liver injuries via optimizing the composition, metabolic pathways and pathogenic replication and secretion of gut microbiota. These findings elucidate the mechanisms of probiotics in alleviating oxidative stress and provide a promising strategy for preventing liver diseases by targeting gut microbiota.