Hepatoprotective effects of fermented field water-dropwort (Oenanthe javanica) extract and its major constituents

•Pretreatment with FDE of t-BHP-intoxicated HepG2 cells inhibited cell death and lactate dehydrogenase (LDH) leakage.•FDE significantly prevented the increase of hepatic enzyme markers (ALT, AST) in vivo.•FDE administration for 7 days significantly affected gene expressions of CYP2E1, CYP4A2, and PPARγ.•Histopathological examination of the livers revealed that FDE reduced the incidence of liver lesions.•Caffeic acid and chlorogenic acid were identified as major constituents of FDE by HPLC, MS, and MS/MS techniques.

Dropwort (Oenanthe javanica) has been used for many years for the treatment of inflammatory conditions, including hepatitis. We investigated the protective effects of fermented field water-dropwort extract (FDE) on tert-butyl hydroperoxide (t-BHP)-induced hepatotoxicity in HepG2 cells and carbon tetrachloride (CCl4)-induced liver damage in rats. Pretreatment with FDE prior to the t-BHP treatment of HepG2 cells inhibited cell death and lactate dehydrogenase (LDH) leakage in a dose-dependent manner. In addition FDE significantly prevented the increase of hepatic enzyme markers (ALT, AST) in vivo. Moreover, FDE administration for 7 days significantly affected CYP2E1, CYP4A2, and PPARγ gene expressions. CYP2E1 and CYP4A2 gene expression in the liver, increased 2 and 22-fold by CCl4 administration, respectively, was attenuated to normal levels by pretreatment with FDE. PPARγ gene expression, completely blocked by CCl4 treatment, was increased by FDE pretreatment compared to normal control group. Histopathological examination of the livers also revealed that FDE reduced the incidence of liver lesions. Caffeic acid and chlorogenic acid were identified as major constituents of FDE. These results demonstrate the protective effects of FDE against hepatocytotoxicity induced by CCl4 and t-BHP in rats and HepG2 cells, thus indicating the potential of FDE as a therapeutic for acute liver diseases.