动物实验,葛根素对,急性肝衰竭 z-bo 2020-09-11 390

　　Objective: To explore the protective effect of puerarin (Pue) on acute liver failure (ALF) induced by D-galactosamine in mice, and to preliminarily observe its mechanism?

　　Methods: Two weeks before modeling, 50 Kangmei mice were randomly divided into 5 groups, Pue group, LY294002 group (LY group), Pue + LY group, 300 mg/kg Pue, 10 mg/kg LY and 300 mg /kg Pue + 10 mg/kg LY, once a day, give the same amount of sterile saline as the normal control group and model group, and fast for 24 hours after the last dose. Except for the normal group, the other groups were given intraperitoneal injection of galactose to establish an ALF model, while the normal control group was given the same amount of sterile saline. For the detection of glutathione peroxidase (GSH-Px) acid aminotransferase (ALT), aspartate transferase (AST), total bilirubin (TBil) levels, malondialdehyde ( MDA) and superoxide dismutase (SOD) kit method content; HE staining? Can TUNEL staining and Western blotting be used to detect pathological changes in mouse liver tissue? Hepatocyte apoptosis and the number of P-Akt? P-GSK-3β? What is the expression level of cleavedcaspase-3 protein?

　　Result: Compared with the model group, the number of apoptotic liver cells in the model group, serum ALT? AST? Tbil level, liver tissue MDA content, cleavedcaspase-3 protein expression level increased significantly (P0.05)?

　　Conclusion: Can Pue activate the PI3K/Akt signaling pathway, thereby reducing the degree of liver damage and protecting the liver of D-galactosamine-induced ALF mice?