Carbon tetrachloride (CCl₄ ) is the main chemical causing liver damage. In this experiment, the effect of Lactobacillus plantarum HFY15 treatment on CCl₄ -induced acute liver injury was investigated using mice. Fifty adult mice were randomized into five study groups, each group with 10 ml kg^-1 saline, 50 mg kg^-1 silymarin, and 10⁹ CFU kg^-1 L. plantarum HFY15 and LDSB per day, and all the mice expect the normal group were injected 0.8% CCl₄ (10 ml kg^-1 ) on the 14th day. Following the 16 h induction of the liver injury, various biochemical markers were assessed for blood and liver tissue. After L. plantarum HFY15 treatment, the content of alanine aminotransferase (ALT), aspartate aminotransferase (AST), triglycerides (TG), malondialdehyde (MDA), and reactive oxygen species (ROS) in serum decreased by 67.7%, 65.0%, 41.9%, 59.5%, and 51.5%, respectively, and the level of antioxidant enzymes (total superoxide dismutation [T-SOD], catalase [CAT], glutathione [GSH]) increased by more than twofold. Pro-inflammatory cytokine interleukin-6 (IL-6), interferon-γ (INF-γ), and tumor necrosis factor-α (TNF-α) decreased by more than 45% in serum and live. What is more, L. plantarum HFY15 increased the expression of antiapoptosis genes Bcl-2 by eightfold, inhibiting the expression of proapoptotic genes Caspase-3 and Bax by about threefold. Lactobacillus plantarum HFY15 has obvious protective effects on CCl₄ -induced liver injury by inhibiting oxidation, reducing the release of inflammatory factors, and exerting suppressive effect on apoptotic process in the CCl₄ -induced liver injury. Lactobacillus plantarum HFY15 can be developed as edible lactic acid bacteria for preventing liver toxicity. PRACTICAL APPLICATION: L. plantarum HFY15 can alleviate liver injury caused by carbon tetrachloride toxicity through antioxidant, anti-inflammatory and anti-apoptotic pathways.

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