Lactobacillus plantarum C88 protects against aflatoxin B1-induced liver injury in mice via inhibition of NF-κB-mediated inflammatory responses and excessive apoptosis

BackgroundProbiotics play an important role in the human and animal defense against liver damage. However, the protective mechanism of Lactobacillus plantarum C88 on chronic liver injury induced by mycotoxin remains unclear.ResultsIn this study, the addition of L. plantarum C88 obviously ameliorated the increased contents of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), total cholesterol and triglyceride, the diminish contents of total protein and albumin in serum of mice challenged with AFB(1). Simultaneously, L. plantarum C88 attenuated the inflammatory response via significantly reducing the levels of pro-inflammatory factors, including interleukin-1 beta (IL-1 beta), IL-6, IL-8, interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) in serum. Furthermore, L. plantarum C88 remarkably down-regulated the nuclear factor kappa B (NF-kappa B) signaling pathways by weakening the expression of toll-like receptor 2 (TLR2) and TLR4, and inhibited NF-kappa B nuclear translocation through enhancing the expression of NF-kappa B inhibitor (I kappa B). Neutralization experiments confirmed that L. plantarum C88 decreased the levels of some pro-inflammatory factors due to the suppression of the NF-kappa B signaling pathways. Besides, L. plantarum C88 decreased the levels of Bax and Caspase-3, elevated the level of Bcl-2, and reduced mRNA expressions of Fatty acid synthetase receptor (Fas), FAS-associated death domain (FADD), TNF receptor associated death domain (TRADD) and Caspase-8 in the liver.ConclusionsProbiotic L. plantarum C88 prevented AFB(1)-induced secretion of pro-inflammatory cytokines by modulating TLR2/NF-kappa B and TLR4/NF-kappa B pathways. The molecular mechanisms of L. plantarum C88 in ameliorating AFB(1)-induced excessive apoptosis included regulating the mitochondrial pathway and cell death receptor pathways.