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(H_2O_2),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 H_2O_2-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 H_2O_2 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. Background Increased reactive oxygen species (ROS) formation, which in turn promotes cardiomyocyte apoptosis, isassociated with the pathogenesis and progression of various cardiac diseases such as ischemia and heart failure. Researches have shown that over expression of heat shock protein 27 (Hsp27) confers resistance to cardiacischemia / reperfusion injury. However, 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. Folly the cells challenged by Hydrogen Peroxide (H 2 O 2), lactate dehydrogenase (LDH) release, apoptosis, intracellular ROS, cell morphology, mitochondrial transmembrane potential and the activation of serine / threonine kinase Akt were determined. Results along with marked suppression of H 2 O 2 -induced injury by Hsp27 Overexpression in H9c2 cells, ROS generation and the loss of mitochondrial membrane potential were also significances antly depressed. Focusmore, AugmentedAkt activation was observed in Hsp27 overexpressed H9c2 cells following H_2O_2 exposure.Conclusions Hsp27 inhibits oxidative stress-induced H9c2 damage and inhibition of ROS generation and the augmentation of Akt activation may be involved in the protective signaling.