Abstract: This study was to investigate the effect and the underlying mechanism of DG on the hepatotoxicity induced by Con A.In this study,a concanavalin A (Con A)-induced hepatitis mouse model was used to examine the effect of DG on hepatic injury.DG(58.5 mg/kg),silymarin (36.4 mg/kg) and bicyclol (9.75 mg/kg) equivalent to clinical dosage were orally administered to mice once daily for 7 consecutive days before Con A challenge.After that,blood samples were collected for serological detection,and histological analysis was carried out by hematoxylin-eosin staining.In order to investigate the molecular mechanism of DG’s protective effect,the serum-drug incubation assay,immunohistochemistry and western blot were conducted.Hematoxylin-eosin staining showed that DG pre-treatment prevented Con A-induced liver structural damage in ICR mice.We also observed the reduced serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities.However,the serum-drug incubation assay indicated that DG cannot directly attenuate ALT and AST levels.Meanwhile,experimental results proved that DG pretreatment down-regulates cleaved Caspase-3,cleaved PARP,ratio of BAX/BCL-2 expression level and expression of TGF-β1,COX-2,IL-6,TNF-α,IFN-γ inflammatory mediators.Taken together,DG can inhibit Con A-induced hepatic injury by inhibition of apoptosis and inflammation.

Key words: diammonium glycyrrhizinate, 18α-GA, concanavalin A, hepatic injury, inflammation, apoptosis