Lipopolysaccharide alleviates liver injury induced by thioacetamide in rats

초록

Lipopolysaccharide (LPS) is the major of outer membrane of gram-negative bacteria and one of the most potent microbial initiators of inflammation. From the previous study showed that exposure to a low dose of LPS renders animals tolerant to a lethal dose of LPS, and protects against the toxicity of some chemicals. However, the effects of LPS treatment in thioacetamide (TA)-induced liver injury remain largely unknown. Liver injury caused by various toxic chemicals such as carbon tetrachloride, alcohol, dimethylnitrosamine. Here, we induced rat liver injury by intraperitoneal injection of TA, a representative hepatic fibrosis inducer. In this study, we investigated the effects of LPS in TA group, LPS group, LPS/TA group and vehicle control group on Sprague-Dawely rats (five rats for each group). All rats at the end of the experiment were sacrificed, and liver and serum were obtained. Serological analysis and hematoxylin and eosin staining showed that LPS/TA cotreatment was associated with decrease of aspartate aminotransferase (AST), alanine transaminase (ALT) and total-bilirubin and fibrosis than in TA-treated rats. RT-PCR showed that the levels of IL-6 and Cox2 mRNA were lower in the liver of LPS/TA-cotreated rats than in TA-treated rats. No significant differences ALT, ALP, AST, total-bilirubin, IL-6 and Cox2 between vehicle control and LPS-treated rats. These results imply that LPS/TA cotreatment partially alleviates the TA-induced liver injury of rats by reducing inflammatory response.

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