Abstract
Background: It has been accounted for that infarct size reduction and cardioprotective effects of Ischemic Postconditioning (IPOC) have been abrogated in few pathological conditions including diabetes. Peroxisome Proliferator-Activated Receptor-Alpha (PPAR-Alpha) agonist is known to have cardioprotective effect. Therefore, the current examination researched the possible role of PPAR-Alpha Agonist in Attenuated Cardioprotective Effects of Ischemic Postconditioning in Diabetic Rat Heart. Materials and Methods: Rats were injected Alloxan Monohydrate (150/mg/kg/i.p) single dose to produced diabetes. Isolated Langendorff ’s perfused normal and diabetic rat hearts were subjected to global ischemia for 30 min followed by reperfusion for 120 min. Coronary effluent was analyzed for Lactatedehydogenase (LDH) and Creatine Kinase (CK) release to evaluate the extent of cardiac injury. The oxidative stress in heart was evaluated by measuring Thiobarbituric Acid Reactive Substances (TBARS), superoxide dismutase (SOD) generation and reduced form of glutathione. Result: In the current investigation, Ischemia-reperfusion (I/R) induced oxidative stress by increasing TBARS, superoxide anion generation and the decreased form of glutathione in normal and diabetic rat heart. Moreover, I/R induced myocardial injury, was evaluated in terms of increase in, LDH and CK release in coronary effluent, and reduction in coronary flow rate in normal and diabetic rat heart. The diabetic rat heart showed enhanced I/R induced myocardial injury with high extent of oxidative stress as compared with normal rat heart subjected to I/R Six episodes of IPOC afforded cardioprotection against I/R induced myocardial injury in normal rat heart as assessed in terms of improvement of coronary flow rate and decrease of LDH, CK and oxidative stress. On other hand, IPOC mediated myocardial protection against I/R injury was nullified in diabetic rat heart. Fenofibrate (5µM), a selective agonist of PPAR alpha, its administration markedly restored the Cardioprotective potential of IPOC in diabetic rat heart. Conclusion: The current investigation presumed that, the high degree of oxidative stress produced in diabetic rat heart during reperfusion and resulting inactivation of PPAR alpha receptor might be responsible for abolishing the Cardioprotective potential of IPOC against I/R induced myocardial injury
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