Mechanisms Of The Delayed Cardioprotection Induced By Hypoxic Preconditioning

lschemic preconditioning (IPC) is a term that is used to describe the phenomenon that brief ischemic episodes can attenuate tissue injury caused by subsequent sustained ischemia/reperfusion. The cardioprotection of IPC has been demonstrated in hypoxic preconditioning (HPC) model of cardiomyocytes. The protection of preconditioning is a biphasic process, including the first protection, which appears shortly after preconditioning and lasts 1 to 3 hours, and the delayed protection, which presents at 12 to 24 hours later and persists 24 to 72 hours. The latter has more clinical significance. Researchers from basic and clinical medicine have paid much attention to find new strategies for prevention and cure of ischemic heart disease through investigating cardioprotective mechanisms of IPC.The research results indicate that the delayed protective mechanisms of HPC involve complicated factors, which includes release of endogeneous protective mediators (adenosine, EDRF and NO), activation of cellular signal transduction systems [protein kinase C (PKC) and mitogen-activated protein kinases (MAPKs)], and the alterations of endogeneous protective proteins in transcription, translation, and post-translation modification (PTM) levels. Among them, the upregulation of endogenous protective proteins is the key event during HPC. However, the exact cellular signal transduction pathway and changes of myocardial proteome involved in HPC have not been fully clearified.The present study testified HPC-induced resistantance to hypoxia/ reoxygenation (H/R) injury in neonatal rat cardiomyocytes, and inveatigated cascades of cell signal transduction and changes of myocardial proteome involved in HPC. The detailed methods as follows.1. In H/R model of neonatal rat cardiomyocytes, we used tampan blue exclusive experiment to test cell necrosis rate. Apoptosis rate was accessed by methods of terminal deoxynucleotidyl transferase-mediate DNA...