Fisetin protects H9c2 cardiomyoblast cells against H2O2-induced apoptosis through Akt and ERK1/2 signaling pathways

Backgrounds: Fisetin (tetrahydroxyflavone), a natural plant component, is known to have different properties including, direct radical scavenger, anti-inflammation, and cell survival. Methods: We investigated whether fisetin can protect cardiomyocytes against H2O2-induced apoptosis that is relevant to cardiovascular disease risks using cell viability test, ROS measurement, and Western blotting. Results: Fisetin decreased apoptotic cell death and intracellular reactive oxygen species (ROS), while enhancing the expression of Cu/Zn-superoxide dismutase (SOD) as well as phosphorylation of Akt and extracellular regulated kinase (ERK) 1/2. In particular, fisetin significantly decreased apoptosis through inhibition of cleaved caspase-3 and Bax expression and by enhancing the expression of anti-apoptotic enzyme as well as Bcl-2 in H2O2-stimulated H9c2 cells. However, the expression of heme oxygenase, catalase, and Mn-SOD was not altered by fisetin in these conditions. Conclusion: Taken together, these data suggest that the potential cardioprotective effect of fisetin may involve Cu/Zn-SOD-mediated activation of Bcl-2 through the Akt and ERK1/2 pathways.