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 μmol/L) significantly enhanced coronary flow, and decreased the pathological scores of myocardium. 50, 100, 200 μmol/L vitexin significantly attenuated I/R-induced increases of myocardial TNF-α and IL-1β, and 25, 50, 100, 200 μmol/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 μmol/L vitexin markedly increased myocardial Bcl-2 protein expression. Furthermore, vitexin at concentrations of 50, 100, 200 μmol/L significantly reduced expression of myocardial NF-κBp65 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-κBp65. Crown