ABSTRACT
Objective:To investigate the effect and mechanism of Sanhuang Yinchi decoction (SHYCD) in preventing carbon tetrachloride (CCl4)-induced acute liver injury by regulating high mobility group box1(HMGB1) signaling pathway. Method:A total of 48 KM mice were randomly divided into blank control group, model group, low, middle and high-dose SHYCD groups and positive control group. The model of acute liver injury induced by CCl4 in mice was established. The low, middle and high-dose SHYCD groups were intragastrically administered with drugs (16, 32, 48 g·kg-1·d-1) respectively, and the positive control group was given cell growth stimulating hormone (20 mg·kg-1·d-1) through intraperitoneal injection. Pathological changes of mouse liver tissue sections were observed by hematoxylin-eosin staining (HE); relevant enzyme kits were used to determine liver function indexes in mice serum-alanine aminotransferase (AST) and aspartate aminotransferase (ALT); the expression level of interleukin-6 (IL-6) in mouse serum was determined by enzyme-linked immunosorbent assay (ELISA); Western blot was used to detect the expressions of high mobility group box-1(HMGB1), cysteine aspartic acid protease(Caspase-3), apoptosis-related molecules B cell lymphoma(Bcl-2), Bcl-2 associated x protein(Bax), and Toll-like receptor 4 (TLR4). Result:Compared with the normal group, the model group significantly increased serum AST, ALT (PPPPPConclusion:SHYCD can prevent liver injury by regulating HMGB1/TLR4/NF-κB signaling pathway, reducing cellular inflammatory response and inhibiting apoptosis, so as to prevent acute liver injury in mice. This indicates that HMGB1 may become a new target to prevent acute liver injury.