Hepatoprotective Effects of Lactobacillus on Carbon Tetrachloride-Induced Acute Liver Injury in Mice

Abstract

The aim of this study was to investigate and compare the effects of heat-killed and live <i>Lactobacillus</i> on carbon tetrachloride (CCl₄)-induced acute liver injury mice. The indexes evaluated included liver pathological changes, the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), superoxide dismutase (SOD), glutathione (GSH), and malondialdehyde (MDA) in the serum, related gene expression (<i>IL-1β</i>, <i>TNF-α</i>, <i>Bcl-2,</i> and <i>Bax</i>), and related proteins levels (Bax, Bcl-2, Caspase 3, and NF-κB p65). Compared with the model group, the results indicated that the levels of ALT, AST, and MDA in the serum, the expression levels of <i>IL-1β</i>, <i>TNF-α,</i> and <i>Bax</i>, and the protein levels of Bax, Caspase 3, and NF-κB p65 significantly decreased, and the pathologic damage degree all significantly reduced after live <i>Lactobacillus fermentum</i> (L-LF) and live <i>Lactobacillus plantarum</i> (L-LP) treatment. Additionally, the levels of SOD and GSH in the serum, the gene expression of <i>Bcl-2</i>, and the protein level of Bcl-2 significantly increased after L-LF and L-LP treatment. Although HK-LF and HK-LP could also have obvious regulating effects on some of the evaluated indexes (ALT, AST, the expression levels of <i>TNF-α</i> and <i>Bax</i>, and the protein level of Bcl-2) and play an important role in weakening liver damage, the regulating effects of L-LF or L-LP on these indexes were all better compared with the corresponding heat-killed <i>Lactobacillus fermentum</i> (HK-LF) and heat-killed <i>Lactobacillus plantarum</i> (HK-LP). Therefore, these results suggested that LF and LP have an important role in liver disease.