Anti-apoptotic and Anti-oxidative Effects of Aqueous Extract prepared from Steamed Daylily Flower in Normal Cardiac and Hepatic Cells against Ethanol

Background: Alcohol abuse resulted in high prevalence of alcoholic cardiac and hepatic disorders. Any agent(s) with the bio-activities to suppress mitochondrial apoptotic pathway, and attenuate apoptotic and oxidative stresses might be able to protect cardiac and hepatic cells against ethanol. Objective(s): Phytochemical composition of aqueous extract prepared from steamed daylily flower (DAE) was determined. The protective effects of DAE for H9c2 and L-02 cells against ethanol were evaluated. Materials and Methods: The amount of total phenolic acids, total flavonoids, total anthocyanins and total triterpenoids in DAE was analyzed. H9c2 or L-02 cells were first treated with 0.25, 0.5 or 1% DAE, and followed by 150 mM ethanol exposure. Results: Results: The amount of total phenolic acids, flavonoids, anthocyanins and triterpenoids in DAE was in the range of 1219-2045 mg/100 g dry weight. DAE treatments at 0.5 and 1% increased the viability of H9c2 cells, but at three test concentrations enhanced the survival of L-02 cells. DAE at 0.5 and 1% up-regulated Bcl-2 mRNA expression, down-regulated Bax mRNA expression, decreased Bax/Bcl-2 ratio, and lowered caspase-3 activity in both cell lines. Ethanol increased reactive oxygen species level, decreased glutathione content, and glutathione peroxidase and catalase activities in both cell lines. DAE at test concentrations reversed these changes in both cell lines. DAE at 0.5 and 1% reduced cytochrome P450 2E1 and NADPH oxidase activities, and lowered p47phox mRNA expression. However, DAE at three test concentrations decreased gp91phox mRNA expression in both cell lines. DAE at 0.5 and 1% up-regulated factor E2-related factor 2 and heme oxygenase-1 mRNA expression in both cell lines. Conclusions: These results suggested that this aqueous extract might be a potent function food supplement to benefit heart and liver against ethanol induced injury.