急性肝衰竭小鼠,葛根素 z-bo 2020-11-25 361

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

　　Methods: 50 Kunming mice were randomly divided into 5 groups. Two weeks before modeling, the Pue group, the LY294002 group (LY group), the Pue+LY group were injected with 300mg/kgPue, 10mg/kgLY and 300mg/kgPue+10mg/ through the tail vein. kgLY, once a day, the normal control group and the model group were given the same amount of sterile normal saline, and fasted for 24 hours after the last administration. Except for the normal group, the other groups were injected intraperitoneally with galactose to construct the ALF model, and the normal control group was injected with the same amount of no Bacterial saline. Biochemical reaction instrument to detect serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (TBil) levels, kit method to detect malondialdehyde in liver tissue (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) content; HE staining, TUNEL staining and Western blotting to detect pathological changes in mouse liver tissues, liver The number of apoptosis and the expression level of P-Akt, P-GSK-3β, cleavedcaspase-3 protein.

　　Results: Compared with the normal control group, the number of apoptotic liver cells, serum ALT, AST, Tbil levels, liver tissue MDA content and cleaved caspase-3 protein expression levels in the model group were significantly increased (P<0.05), SOD, GSH-Px content and P-Akt､P-GSK-3β protein expression levels were significantly decreased (P<0.05); after treatment in the Pue group, compared with the model group, the changes in each index in the Pue group were significantly improved (P<0.05) ly="" p="">0.05).

　　Conclusion: Pue may activate the PI3K/Akt signaling pathway, thereby reducing the degree of liver damage, and exerting a protective effect on the liver of D-galactosamine-induced ALF mice.