Objective: To investigate the protective effect of puerarin on D-galactosamine-induced acute liver failure (ALF) in mice and to preliminarily observe its mechanism.
Methods: Fifty Kunming mice were randomly divided into 5 groups. Two weeks before modeling, the Pue group, the LY294002 group (LY group), and the Pue+LY group were injected with 300mg/kgPue, 10mg/kgLY and 300mg/kgPue+10mg/kg via tail vein injection. kgLY, once a day, the normal control group and the model group were given the same amount of sterile saline, and fasted for 24 hours after the last administration. Except for the normal group, the other groups were injected with galactose intraperitoneally to build the ALF model. The normal control group was injected with the same amount of no food. The levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and total bilirubin (TBil) in serum were detected by biochemical reaction instrument, and malondialdehyde in liver tissue was detected by kit method. (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) content; HE staining, TUNEL staining and Western blotting were used to detect the pathological changes of mouse liver tissue, liver The number of apoptotic cells and the protein expression levels of P-Akt, P-GSK-3β and cleavedcaspase-3.
Results: Compared with the normal control group, the apoptotic number of hepatocytes, serum ALT, AST and Tbil levels, MDA content in liver tissue and expression of cleaved caspase-3 protein were significantly increased in the model group (P<0.05). The content of GSH-Px and the expression levels of P-Akt and P-GSK-3β protein were significantly decreased (P<0.05); after treatment in the Pue group, compared with the model group, the changes of each index in the Pue group were significantly improved (P<0.05). ly="" p="">0.05).
Conclusion: Pue may reduce the damage of liver function by activating the PI3K/Akt signaling pathway, and exert a protective effect on the liver of D-galactosamine-induced ALF mice.