A Synthetic Polyphenol Limits Hydrogen Peroxide-Induced Cell Death in H9c2 Myocyte-like Cells

摘要

Myocardial ischemia-reperfusion (IR) injury stimulates hydrogen peroxide (H_2O_2) accumulation that contributes to cardiac myocyte damage by enhancing apoptosis and necrosis. Antioxidants that inhibit damaging ROS have been proposed as a potential treatment option. Our data demonstrates that a synthetic polyphenol (bisphenol; BP) enhances viability of cultured H9c2 cells exposed to pathologic H_2O_2. Added tBP decreased cellular ROS production stimulated by added H_2O_2 in a dose-dependent fashion. This decreased oxidative stress, inhibited mitochondrial dysfunction, reversed ATP depletion, and ameliorated the H_2O_2-induced increase in apoptosis and necrosis. These data indicate a potential cardio-protective activity for tBP that requires verification in experimental animal models AMI.