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KMID : 1034820180140020183
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Molecular & Cellular Toxicology
2018 Volume.14 No. 2 p.183 ~ p.192
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Fisetin protects H9c2 cardiomyoblast cells against H2O2-induced apoptosis through Akt and ERK1/2 signaling pathways
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Lee Jeong-Soo
Lee Ji-Sook
Cha Kyung-Jae
Kim Dae-Eun
Lee Da-Ye
Jung Sun-Young
Park Eun-Seok
Kim In-Sik
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Abstract
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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.
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KEYWORD
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Fisetin, Oxidative stress, Myocardial apoptosis, Akt, ERK1/2
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