Fisetin protects H9c2 cardiomyoblast cells against H2O2-induced apoptosis through Akt and ERK1/2 signaling pathways
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Fisetin (tetrahydroxyflavone), a natural plant component, is known to have different properties including, direct radical scavenger, anti-inflammation, and cell survival.
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.
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.
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.
KeywordsFisetin Oxidative stress Myocardial apoptosis Akt ERK1/2
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