Vitexin protects against myocardial ischemia/reperfusion injury in Langendorff-perfused rat hearts by attenuating inflammatory response and apoptosis

The aim of the present study is to investigate the effects and its possible underlying mechanisms of vitexin on myocardial ischemia/reperfusion (I/R) injury in isolated rat hearts. Isolated rat hearts were perfused with Langendorff apparatus, which subjected to 30 min ischemia and then followed by 60 min reperfusion. In the isolated rat heart subjected to I/R injury, treatment of vitexin (50, 100, 200 mu mol/L) significantly enhanced coronary flow, and decreased the pathological scores of myocardium. 50, 100, 200 mu mol/L vitexin significantly attenuated I/R-induced increases of myocardial TNF-alpha and IL-1 beta. and 25, 50, 100, 200 mu mol/L vitexin significantly reduced apoptosis index of cardiac muscle cell of rat isolated heart subjected to I/R injury. Vitexin significantly inhibited I/R-induced increase of myocardial Bax protein expression; however, 100, 200 mu mol/L vitexin markedly increased myocardial Bcl-2 protein expression. Furthermore, vitexin at concentrations of 50, 100, 200 mu mol/L significantly reduced expression of myocardial NF-kappa Bp65 protein. Therefore, these results demonstrate that vitexin exhibits significant protective effect against myocardial I/R injury in isolated rat heart, which is related to inhibition of the release of inflammatory cytokines and the apoptosis of cardiac muscle cell via up-regulating protein expression of Bcl-2 as well as down-regulating Bax and NF-kappa Bp65. Crown Copyright (C) 2011 Published by Elsevier Ltd. All rights reserved.