The Effects Of Remote Ischemic Preconditioning And Remote Ischemic Postconditioning To The Expression Of Protein Molecules

Objective:Ischemic heart disease is becoming the leading threat to people's health. And the major manifestation is acute myocardial infarction, which requires emergency revascularization using either fibrinolytic therapy or primary percutaneous coronary intervention (PPCI) to restore the blood flow. In all these cases, the heart is subjected to acute ischemia-reperfusion injury. Innovative treatment strategies for protecting myocardium against the detrimental effects of this form of injury are required to improve the clinical outcomes in patients. In this regard, lots of researches had showed that the endogenous protection elicited by the heart's ability to "condition" itself has emerged as a powerful protective method against the ischemia-reperfusion injury. The phenomenon called "ischemic preconditioning" was first discovered by Murry in 1986,and Zhao first introduced "ischemic postconditioning" in 2003. Subsequently, "remote ischemic preconditioning and remote ischemic postconditioning" had been discovered in different organs. All these protective strategies depend on stimulation of the cell signal pathways. Phosphorylation of P38 MAPK and ERK(1/2) during the "preconditioning or postconditioning" and cell protection by HSP27, BCL-2 had been confirmed in the past decades. The purpose of this article is to observe whether BCL-2 expression,the phosphorylation of P38 MAPK, ERK(1/2) and HSP27 has been changed during "remote ischemic preconditioning and remote ischemic postconditioning".Methods:Health Male gerbils(weight 60-70g) were randomly assigned to six groups(group A-F,n=6).Control (group A) just exposed carotid artery; I/R (group B) was subjected to 30min unilateral CAO followed by 1h of reperfusion; RIPC (group C) was elicited by three cycles 3min unilateral CAO plus 2min reperfusion before the 30min occlusion period; RIPost (group D)was elicited by three cycles 10s reperfusion, followed by 10s reocclusion after the 30min unilateral CAO period and before the 1h reperfusion; RIPC(group E) occlude bilateral carotid artery, the right carotid artery was underwent three cycles of CAO for 3min followed by 2min of reperfusion, then bilateral carotid artery reperfusion for 1h;RIPC (group F)similar to groupC but occlude the other side carotid artery which was not subject to ischemic preconditioning. Myocardial tissue samples were obtained directly after the procedure and snap frozen in liquid nitrogen, stored at-70℃,protein extracted and using western blot to detect BCL-2 and phosphorylated P38 MAPK, ERK(1/2), HSP27.Results:Phosphorylated P38 MAPK increased a lot in I/R group (P<0.05),in RIPC and RIpost obviously decrease phosphorylated P38 MAPK compared with I/R group.Phosphorylated HSP27 slightly increased in I/R group, but highly increased in RIPC and RIpost. ERK(1/2) had been strongly phosphorylated in I/R group compare with the Control group, there are differences in ERK1 phosphorylation between each group(P<0.05), but there are not any obvious changes in ERK2 between I/R group and RIPC or RIpost group.BCL-2 expression increased in the I/R group, and apparently higher in RIPC and RIpost group than I/R group.Conclusion:Remote ischemic preconditioning and remote ischemic postconditioning can change the P38 MAPK, ERK(1/2), HSP27 phosphorylation and expression of BCL-2 in the heart. The mechanism of protective effect conducted by remote ischemic preconditioning and remote ischemic postconditioning may contribute to the changes in P38 MAPK, ERK(1/2), HSP27 phosphorylation and BCL-2 expression in the target organ.