Objective To study the intervention effect of emodin on Con A-induced acute liver injury in mice and the underlying mechanism. Methods The male Balb/C mice were randomly divided into the control group, model group, and emodin group. Emodin(25 mg/kg) was administered orally, and Con A(20 mg/kg) was given through intravenous injection at 2 h after emodin administration in the emodin group. In place of emodin, CMC-Na was used in the model group, and mice in the control group were not treated.After 10 h of Con A injection, the blood was collected from the retro-orbital sinus in mice and the serum levels of ALT and AST were measured. Hepatic sections were aseptically obtained for histopathological examination to assess the degree of liver damage. The real-time fluorescent quantitative PCR and Western blotting were employed to evaluate the expression of glucocorticoid-induced tumor necrosis factor receptor(GITR) mRNA and its ligand GITRL mRNA.Results The serum ALT and AST levels in the model group were significantly higher than those in the control group, while those in the emodin group were lower than those in the model group(all P<0.01). Compared with the control group, there were more significant necrosis foci in the liver tissues of the model group, while the liver necrosis was significantly reduced in the emodin group. The relative expression levels of GITR and GITRL mRNA in the model group were higher than those in the control group, while the relative expression levels of GITR and GITRL mRNA in the emodin group were lower than those in the model group(all P<0.05). The relative expression levels of GITR and GITRL protein in the model group were higher than those in the control group, while the relative expression levels of GITR and GITRL protein in the emodin group were lower than those in the model group(all P<0.05). Conclusion Emodin alleviates Con A-induced liver damage by inhibiting GITR/GITRL pathway. [ABSTRACT FROM AUTHOR]