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Dioscorea bulbifera L., a traditionally used medicinal plant in China, is reported to induce hepatotoxicity. The present study is designed to investigate the protection of an ethanol extract of Angelica sinensis (Oliv) Diels (AE) against an ethyl acetate fraction of D. bulbifera (EF)-induced liver injury and its engaged mechanism. High performance liquid chromatography (HPLC) analysis showed that the amount of diosbulbin B in EF was 16.03% and ferulic acid in AE was 0.18%. EF (350 mg/kg) increased serum alanine/aspartate aminotransferase (ALT/AST), alkaline phosphatase (ALP) activities and total bilirubin (TB) amount, while AE inhibited such an increase. Liver histological evaluation showed that AE prevented development of severe hepatic lesions induced by EF. Further results showed that EF decreased the expression of Bcl-2 and induced the cleaved activation of caspase-9 and -3, and all those effects were reversed by AE. AE also reversed EF-induced decreased expression of the inhibitor of kappa B (IκB), superoxide dismutase (SOD), and glutathione peroxidase (GPx). Taken together, our results demonstrate that AE can prevent EF-induced hepatotoxicity via preventing apoptosis, meanwhile IκB, SOD, and GPx may be involved in such protection.

Protection of Angelica sinensis (Oliv) Diels against hepatotoxicity induced by Dioscorea bulbifera L. and its mechanism