Antioxidative and hepatoprotective activities of the ethyl acetate fraction separated from the fruit of Livistona chinensis.

To examine the antioxidative and hepatoprotective activities of the effective fraction separated from the fruit of Livistona chinensis (FLC) and to explore the possible mechanism.The antioxidative activities of the various fractions separated from FLC were analyzed by in vitro DPPH (1,1-diphenyl-2-picrylhydrazyl radical 2, 2-diphenyl-1-(2,4,6-trinitrophenyl) hydrazyl, DPPH) radical and superoxide anion free radical (O2- scavenging assays. The potential hepatoprotective effects of the ethyl acetate fraction separated from FLC (EFLC) were examined in LO2 cells and mice. LO2 cells were incubated with EFLC and exposed to H2O2-induced oxidative stress. BABL/C mice were orally administered EFLC for consecutive 7 d, and fulminant hepatitis was induced by cauda vein injection of ConA on day 7.EFLC showed prominent antioxidative effects in DPPHï¼?and O2ï¼?scavenging assays. EFLC pretreatment effectively protected LO2 cells from H2O2-induced oxidative stress by decreasing apoptosis and raising the levels of antioxidant enzymes. Additionally, EFLC protected mice against ConA-induced fulminant hepatitis by markedly reducing the serum levels of alanine transaminase and aspartate aminotransferase, attenuating histological damage of the mouse liver, and elevating the levels of glutathione peroxidase and total superoxide dismutase, while decreasing the contents of methane dicarboxylic aldehyde, tumor necrosis factor-¦Á, and interleukin-1¦Â in the mouse liver. Furthermore, EFLC pretreatment downregulated the protein expression of B-cell lymphoma 2 (Bcl-2) associated X protein, caspase-3, caspase-8, Fas, and FasL, while upregulating the protein expression of Bcl-2 in the mouse liver.These findings revealed that EFLC effectively protected against in vivo and in vitro liver injury, and the mechanism is closely associated with its antioxidative and anti-apoptotic properties.