Abstract
The present study aimed to investigate the possible role of JAK-2 in attenuated cardio protective effects of ischemic post-conditioning (IPOC) in Hyperglycaemic rat heart. Experimental hyperglycaemia was induced by Alloxan monohydrate (100 mg/kg, i.p). Isolated normal & hyperglycaemic rat heart mounted on Langendorff's apparatus was subjected to 30 min of global ischemia followed by 120 min of reperfusion. Six episodes of ischemia followed by reperfusion with Kreb's-Henseleit solution were given each comprising of 10 s to produce IPOC. Ischemia-reperfusion (I/R) induced oxidative stress by increasing thiobarbituric acid reactive substances (TBARS), superoxide-dismutase (SOD) and decreasing reduced form of glutathione in normal and hyperglycaemic rat heart. Furthermore, I/R induced myocardial injury which were indexed by increased in LDH, CK-MB release in coronary effluent, myocardial infract size, and decreased in coronary flow rate in normal and hyperglycaemic rat heart. Extent of myocardial injury was measured in terms of infarct size by triphenyltetrazolium chloride (TTC) staining. The hyperglycaemic rat heart showed enhanced I/R-induced myocardial injury with noted high degree of oxidative stress. Treatment with Tyrphostin-AG490 (5 μM), a selective inhibitor of JAK-2 markedly restored the cardioprotective potential of IPOC in hyperglycaemic rat heart. The high degree of oxidative stress produced in hyperglycaemic rat hearts during reperfusion may activate JAK-2, which may be implicated in the observed paradoxically abrogated cardioprotective effect of IPOC. It is concluded that the high degree of oxidative stress produced in hyperglycaemic rat heart during reperfusion may activate JAK-2, may be implicated in the observed paradoxically abrogated cardioprotective effect of IPOC.
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