%0 Journal Article
%T Antiapoptotic Actions of Methyl Gallate on Neonatal Rat Cardiac Myocytes Exposed to H2O2
%A Sandhya Khurana
%A Amanda Hollingsworth
%A Matthew Piche
%A Krishnan Venkataraman
%A Aseem Kumar
%A Gregory M. Ross
%A T. C. Tai
%J Oxidative Medicine and Cellular Longevity
%D 2014
%I Hindawi Publishing Corporation
%R 10.1155/2014/657512
%X Reactive oxygen species trigger cardiomyocyte cell death via increased oxidative stress and have been implicated in the pathogenesis of cardiovascular diseases. The prevention of cardiomyocyte apoptosis is a putative therapeutic target in cardioprotection. Polyphenol intake has been associated with reduced incidences of cardiovascular disease and better overall health. Polyphenols like epigallocatechin gallate (EGCG) can reduce apoptosis of cardiomyocytes, resulting in better health outcomes in animal models of cardiac disorders. Here, we analyzed whether the antioxidant N-acetyl cysteine (NAC) or polyphenols EGCG, gallic acid (GA) or methyl gallate (MG) can protect cardiomyocytes from cobalt or H2O2-induced stress. We demonstrate that MG can uphold viability of neonatal rat cardiomyocytes exposed to H2O2 by diminishing intracellular ROS, maintaining mitochondrial membrane potential, augmenting endogenous glutathione, and reducing apoptosis as evidenced by impaired Annexin V/PI staining, prevention of DNA fragmentation, and cleaved caspase-9 accumulation. These findings suggest a therapeutic value for MG in cardioprotection. 1. Introduction Reactive oxygen species (ROS), a product of normal cellular metabolism, are usually handled effectively by the cellular defense systems, thereby having little bearing on cellular health. Cellular redox balance is maintained by antioxidant enzymes, such as superoxide dismutase and catalase, and by signaling mechanisms to conserve a state of oxidative homeostasis. However, under situations of exaggerated stress or hypoxia, the cellular defenses may be insufficient to overcome ROS overload. Oxidative stress has been clinically shown to be relevant in the progression of cardiac diseases and heart failure [1, 2]. Excess ROS can cause a variety of cellular damage including mitochondrial dysfunction, DNA damage, and ultimately lead to apoptosis with apoptosis of cardiomyocytes being critical in tissue damage and eventually heart failure. Hence, protection of cardiomyocytes and their increased survival is a putative target for cardioprotection [3]. Increasing evidence suggests that fetal hypoxia and resultant increased ROS are factors that can program for adult diseases, a phenomenon known as developmental programming; the activation of oxidative stress pathways in utero can program for cardiac dysfunction in adulthood such as responses to ischemia/reperfusion, cardiac function, coronary flow, and hypertension [4¨C7]. Hypoxia due to intrauterine stress during fetal development affects cardiogenesis and can have adverse
%U http://www.hindawi.com/journals/omcl/2014/657512/