# Bacillus amyloliquefaciens BA5 Attenuates Carbon Tetrachloride-Induced Hepatotoxicity in Mice

## TL;DR

This study shows that Bacillus amyloliquefaciens BA5 can protect mice from liver damage caused by carbon tetrachloride by reducing oxidative stress and improving gut health.

## Contribution

The study demonstrates the protective effects of BA5 on CCl4-induced liver injury through antioxidant activity and gut microbiota modulation in mice.

## Key findings

- BA5 reduced oxidative stress markers and improved antioxidant levels in CCl4-treated mice.
- BA5 restored liver and intestinal tissue damage caused by CCl4 exposure.
- BA5 increased beneficial gut bacteria and decreased harmful bacteria, enhancing gut microbial diversity.

## Abstract

Background: The association between liver disease and gut microbiota is being widely investigated. Probiotics, such as Bacillus amyloliquefaciens, are among the most notable microbiomes examined in this study. Bacillus amyloliquefaciens shows potential for promoting growth and effectively regulating gut microbiota, though its mechanism of action remains unclear. Methods: The early gavage administration of Bacillus amyloliquefaciens BA5 conferred protection against liver injury in carbon tetrachloride (CCl4)-induced mice. Growth parameters (body weight and organ index), serum biochemical markers (ALT, AST, T-SOD, MDA, GSH-Px, and T-AOC), liver and jejunum histopathology, and gut microbiota composition were comprehensively evaluated. Results: BA5 supplementation restored serum T-AOC, T-SOD, and GSH-Px levels and attenuated CCl4-induced increases in ALT, AST, and MDA, suggesting potent anti-oxidant properties. Furthermore, histopathologic assessment showed that CCl4-induced mice developed acute liver injury and intestinal villi were destroyed, while the BA5 group restored the pathological changes in the tissues to the normal group level. In addition, immunohistochemical staining revealed that BA5 increased the expression level of Claudin-1 which was a key biomarker for assessing the integrity of epithelial/endothelial barriers. Regarding gut microbiota, BA5 significantly enhanced the abundance of beneficial bacteria (Lactobacillus) and decreased the abundance of hazardous bacteria (Fusobacterium, Lachnoclostridium, Phascolarctobacterium, and Escherichia–shigella) caused by CCl4. Notably, BA5 alone remarkably increased gut microbial diversity compared with that of the Control group. Conclusions: Overall, these findings suggest that BA5 holds promise as a potential therapeutic agent for alleviating CCl4-induced acute liver injury in mice by mitigating oxidative stress and modulating gut microbiota.