Objective: To study the protective effect of baicalin solid dispersion (BSD) on D-galactosamine (D-GalN) induced acute hepatic injury in mice, and to compare it with baicalin alone.
Methods: Sixty mice were randomly divided into six groups, i.e., the normal control group, the D-GalN model group, the bifendate group (at the daily dose of 200 mg/kg), the baicalin group (at the daily dose of 50 mg/kg), the low dose BSD group (at the daily dose of 50 mg/kg), and the high dose BSD group (at the daily dose of 100 mg/kg), 10 in each group. 0.5% CMC-Na at 20 mL/kg was administered to mice in the normal group and the model group by gastrogavage, while corresponding medication was administered to mice in the other three groups by gastrogavage. Seven days after administration, acute hepatic injury model was induced by intraperitoneal injection of D-GalN. The liver index and the spleen index were calculated. The serum activities of alanine aminotransferase (ALT) and asparate aminotransferase (AST), the contents of superoxide dismutase (SOD) and malondialdehyde (MDA) in the liver homogenate were measured. The pathological changes of the liver tissue were observed by HE staining.
Results: Compared with the normal control group, widespread inflammation and necrosis was significant in the liver tissue of the D-GalN model group; the liver index, serum ALT and AST levels and hepatic MDA content obviously increased, hepatic SOD activity decreased, showing statistical difference (P < 0.05). Compared with the model group, the liver index, the serum levels of ALT and AST, and hepatic MDA decreased, hepatic SOD increased, the degree of hepatic tissue injury was significantly improved in the low dose and high dose BSD groups. Besides, better effects were obtained in the low dose BSD group than in the baicalin group with statistical difference (P < 0.05).
Conclusion: BSD could significantly protect D-GalN induced acute hepatic injury of mice, and its effect was superior to that of baicalin alone.