Heat shock protein 27 regulates oxidative stress-induced apoptosis in cardiomyocytes:mechanisms via reactive oxygen species generation and Akt activation

摘要

＜正＞ Background Increased reactive oxygen species（ROS）formation,which in turn promotes cardiomyocytes apoptosis,isassociated with the pathogenesis and progression of various cardiac diseases such as ischemia and heart failure.Recent studies have shown that over expression of heat shock protein 27（Hsp27）confers resistance to cardiacischemia/reperfusion injury.However,not much is known about the regulation of myocyte survival by Hsp27.Methods The rat cardiac cell line H9c2,with a stable overexpression of Hsp27,was established,with empty vectortransfected H9c2 cells as controls.Following the cells challenged by Hydrogen Peroxide（H2O2）,lactate dehydrogenase（LDH）release,apoptosis,intracellular ROS,cell morphology,mitochondrial transmembrane potential and the activationof serine/threonine kinase Akt were determined.Results Along with marked suppression of H2O2-induced injury by Hsp27 overexpression in H9c2 cells,ROSgeneration and the loss of mitochondrial membrane potential were also significantly depressed.Furthermore,augmentedAkt activation was observed in Hsp27 overexpressed H9c2 cells following H2O2 exposure.Conclusions Hsp27 inhibits oxidative stress-induced H9c2 damage and inhibition of ROS generation and theaugmentation of Akt activation may be involved in the protective signaling.