| Objective To explore the protective role for Adenosine-5’-triphosphate (ATP) post conditioning of PI3-kinase-Akt-endothelial nitric oxide synthase (PI3K-Akt-eNOS) signaling pathway on myocardial ischemia reperfusion injury (IRI) in experimental rabbits. Methods The IRI model was established in New Zealand white male rabbits and the animals were divided into4groups.①Control group,the rabbits with ischemia reperfusion(IR),②ATP group, IR rabbits received ATP post conditioning,③Wortmannin+ATP group, IR rabbits were treated with PI3-kinase inhibitor wortmannin and ATP post conditioning,④5-HD+ATP group, IR rabbits were treated with mitochondrion ATP-sensitive K+channel (mitoKATP) pathway inhibitor5-HD and ATP post conditioning.The myocardial pathological changes were observed by HE staining,the myocardial cell apoptosis was determined by TUNEL method,the expression of Bcl-2,Bax,the ratio of Bcl-2/Bax and p-eNOS were examined by immunohistro-chemistry method. Results Compared with Control group, the ATP group showed less smaller of myocardial cell nuclear and tissue edema, reduced apopsis index and increased ratio of Bcl-2/Bax,all p＜0.01.In both Wortmannin+ATP group and5-HD+ATP group,the size of myocardial cell nuclear and the condition of tissue edema were similar to Control group,the myocardial cell apoptosis index and ratio of Bcl-2/Bax were similar to Control group, p＞0.05.Compared with Control group and Wortmannin+ATP group,the p-eNOS protein positive expression was significally increased in ATP group, p＜0.01and it was similar to5-HD+ATP group, p＞0.05.Conclusion ATP post conditioning may activiate PI3K-Akt-eNOS signaling pathway, work on mitoKATP pathway,to reduce cell apopsis and IRI in experimental rabbits. |
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