Protective effects of Bacillus clausii against Amoxicillin-induced hepatic injury are associated with Attenuation of LPS-TLR4-NF-κB signalling.

Amoxicillin (AMX) is a widely used β-lactam antibiotic that can cause liver injury through oxidative stress and inflammation, often disrupting the gut-liver axis. This study explored the hepatoprotective effects of the probiotic Bacillus clausii (B. clausii, BCL) in male Swiss albino mice divided into four groups: control, BCL, AMX, and AMX + BCL, with treatments administered orally for 45 days.AMX treatment led to significant liver dysfunction, evidenced by elevated aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and tumor necrosis factor-alpha (TNF-α), together with increased oxidative stress markers and decreased antioxidant defenses. Co-administration of BCL significantly reduced liver enzyme activities, partially restored antioxidant defenses, and decreased inflammatory mediators, including TNF-α and nuclear factor kappa B (NF-κB). Histopathological analyses may reflect reduced liver injury and downregulation of Toll-like receptor 4 (TLR4) signalling in the combination group. BCL alone enhanced liver safety and antioxidant capacity. BCL demonstrated substantial hepatoprotection against AMX-induced liver damage by mitigating oxidative stress and inflammatory pathways, highlighting its potential as a therapeutic probiotic in antibiotic-associated hepatic injury.