| Aim: To investigate the protective effect and mechanism of ligustrazin precondition- ing against myocardial ischemia-reperfusion injury.Methods:fifty rats were divided into five groups randomly: normal group, ischemia-reperfusion group. preconditioning group(IP group), ligustrazine group, ligustrazine+5-HD (The inhibitor of mitochondrial ATP- sensitive potassium channel 5-Hydroxydecanoate) group. The preconditioning protocol consisted of 3 cycle of 10 minutes ischemia and 3 cycle of 10 minutes reperfusion. The rats were subjected to 30 minutes of local ischemia followed by 60 minutes of reperfusion. The infract size was measured by nitroblue titrazolium and red tetrazolium staining. Examine the content of CK and LDH in blood. The ultra structural change of the myocardium was observed under electronmicroscope. Inspect cardiac function of ligustrazine group and ligustrazine+5-HD group during reperfusion. The myocardial cell apoptosis was determined with terminal deoxynucleotidyl trnasferase-mediated dUTP-fluoresce in nick end labeling(TUNEL) method.Results: IP group, ligustrazine group could result in marked reduction of infract size, the content of CK and LDH examined in blood was lower than ischemia-reperfusion group and ligustrazine+5-HD group. The significant ultra structural change were mitochondrial swelling and damage of capillary endothelium, which are more severe in Is chemia-reperfusion group and ligustrazine+5-HD group than IP group and ligustrazine group. Compared with ischemia-reperfusion group and ligustrazine+5-HD group, IP group and ligustrazine group obviously decreases myocardial apoptosis .Conclusion: the heart of ligustrazine preconditioning have protective effect against myocardial ischemia-reperfusion injury, the one of mechanisms is opening mitochondrial ATP- sensitive potassium channel. |
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