Abstract: Objective To investigate the effects of emodin on hepatocyte injury and hepatic inflammation in non-alcoholic steatohepatitis (NASH) rats based on Sirtuin 3 (SIRT3)/forkhead box O1 (FOXO1) signaling pathway.Methods A total of 100 Sprague-Dawley rats were randomly divided into 5 groups, including control group, model group, low-, medium- and high-dose emodin groups. NASH models were established by feeding high-fat diets for 12 weeks. And then 3 emodin groups received the corresponding treatments, while the control group and model group were given the same volume of normal saline. At the end of the experiment, hepatic steatosis, inflammation, ballooning degeneration and nonalcoholic fatty liver disease activity score (NAS) were evaluated, and many other indexes were detected, including levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), messenger ribonucleic acid, expression of SIRT3, FOXO1, caspase-3, caspase-6, and caspase-9 in rat liver tissues.Results The scores of steatosis, inflammation and ballooning degeneration, NAS, levels of AST, ALT, TNF-α, IL-6, caspase-3, caspase-6, and caspase-9 in 3 emodin groups were lower than those in model group. With the increase of the dosage of emodin in each dose group, the scores and levels gradually decreased. While the mRNA and protein levels of SIRT3 and FOXO1 in 3 emodin groups were higher than those in model group. The higher dose emodin the rats had received, the higher the expression levels of SIRT3 and FOXO1 became. Furtheremore, all the parameters changed in a dose-dependent manner (P<0.05).Conclusion Emodin reduce the hepatic inflammation and hepatocyte apoptosis, and alleviate hepatocytes injury in NASH rats through increasing the expression of SIRT3 and FOXO1.

Key words: Emodin, Non-alcoholic steatohepatitis, Sirtuin 3/forkhead box O1 signaling pathway