Limosilactobacillus fermentum XY18 Relieves CCl4-Induced Acute Liver Injury in Mice by Antioxidant and Anti-Inflammatory

Abstract

This study investigated whether Limosilactobacillus fermentum XY18 (LF-XY18) prevents carbon tetrachloride (CCl₄)-induced mice acute liver injury (ALI) by alleviating oxidative stress and inflammation. LF-XY18 reduced liver weight, improved injury indices, and alleviated histological abnormalities in mice. LF-XY18 significantly reduced serum alanine triglycerides (TG), aspartate aminotransferase (AST), total cholesterol (TC), and aminotransferase (ALT) levels and reduced the myeloperoxidase (MPO) and malondialdehyde (MDA) concentrations in both serum and liver tissues, while increasing glutathione (GSH) and superoxide dismutase (SOD) levels in these compartments. Moreover, LF-XY18 activated the nuclear factor-erythroid-2-related-factor-2 (Nrf2) antioxidant pathway, upregulating heme oxygenase-1 (HO-1), copper-zinc superoxide dismutase (Cu/Zn-SOD), manganese-superoxide dismutase (Mn-SOD), and glutathione peroxidase (GSH-Px). Simultaneously, LF-XY18 modulated the nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB)-mediated inflammatory responses, restoring the NF-κB, B-cell inhibitor-α (IκB-α), neuronal nitric oxide synthase (nNOS), endothelial NOS (eNOS), inducible NOS (iNOS), and cyclooxygenase-2 (COX-2) expressions. LF-XY18 dose-dependently ameliorated CCl₄-induced ALI through oxidative stress and inflammation suppression, demonstrating probiotic properties suitable for development as hepatoprotective dietary supplements.