Lactobacillus fermentum HFY06 reduced CCl₄-induced hepatic damage in Kunming mice

This study was conducted to investigate the preventative effect of Lactobacillus fermentum HFY06 on carbon tetrachloride (CCl₄)-induced liver injury in Kunming mice. Mice were treated with HFY06, then liver damage was induced using CCl₄. Evaluation indicators included the activities of aspartate aminotransferase (AST), triglycerides (TG), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and malondialdehyde (MDA) in serum; cytokines levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) in serum; and related gene expressions of nuclear factor-κB (NF-κB), TNF-α, cyclooxygenase-2 (COX-2), copper/zinc superoxide dismutase (Cu/Zn-SOD), manganese superoxide dismutase (Mn-SOD), and catalase (CAT). Liver tissue was stained with hematoxylin and eosin for pathological analysis. Compared with the model group, HFY06 reduced the liver index, increased the serum SOD and GSH-Px activities, and reduced the AST, TG, and MDA activities in the mice. Inflammation-related IL-6, TNF-α and IFN-γ levels were also reduced after treatment with a high dose of HFY06. Pathological observation showed that CCl₄ damaged the mouse livers, which were significantly improved after treatment with silymarin and HFY06. qPCR also confirmed that the high dose of HFY06 (10⁹ colony-forming units [CFU] per kg per day) upregulated the mRNA expression of the antioxidant genes, Cu/Zn-SOD, Mn-SOD, and CAT, in the liver tissue and downregulated the mRNA expression of the inflammatory factors, NF-κB, TNF-α and COX-2, but HFY06 was less effective than silymarin. These findings indicate that HFY06 prevented CCl₄-induced liver damage in vivo but was less effective than silymarin. Thus, HFY06 may have a potential role in treating liver diseases.