p38 MAPK在瑞芬太尼预处理对心脏缺血再灌注损伤保护机制中的角色  

Protective effect of remifentanil preconditioning on myocardial ischemia reperfusion injury in rat hearts:role of p38 mitogen-activated protein kinases

作　　者：张野[1] 顾尔伟[1] 张健[1] 赵庆[1] 陈志武[2] 

机构地区：[1]安徽医科大学第一附属医院麻醉科,合肥市230022 [2]安徽医科大学药理学教研室,合肥市230022

出　　处：《国际麻醉学与复苏杂志》2006年第5期257-260,共4页International Journal of Anesthesiology and Resuscitation

摘　　要：Objective To assess the role of p38 MAPK in protective effect of remifentanil preconditioning(RPC) on myocardial ischemia reperfusion injury in rat hearts.Methods Male Spargue-Dawley rats weighing 300 g to 350 g were used.They were randomly assigned to 1 of 8 groups: Control(CON,saline vehicle),SB 203580(SB,a p38 MAPK inhibitor),RPC,ischemia preconditioning(IPC),SB+RPC,SB+IPC, RPC+SB and IPC+SB.Infarct size(IS),a percentage of the area at risk(AAR),was determined by triphenyltetrazolium(TTC) staining.Tissue simple were processed from the entire AAR of left ventricle for the determination of p38 MAPK protein expression(5 hearts/group).The bands representing the proteins were visualised using an enhanced chemiluminescence detection system.Results IS/AAR was reduced by IPC or RPC,compare to CON.SB administered prior to PC abolished effect of IS/AAR reduction of IPC but RPC Treatment of SB prior to sustained ischemia diminished both protective effect of RPC and IPC on IS/AAR.In IPC group,phospho-p38 MAPK protein increased significantly within 5 min ischemia and remained elevating at 30 min reperfusion,while phospho-p38 MAPK protein in RPC increased significantly at 30 min reperfusion only.Conclusion The activation of p38 MAPK acts as a mediator of RPC,while it may have trigger and mediator effects in IPC.Objective To assess the role of p38 MAPK in protective effect of remifentanil preconditioning（RPC） on myocardial ischemia reperfusion injury in rat hearts. Methods Male Spargue-Dawley rats weighing 300 g to 350 g were used. They were randomly assigned to 1 of 8 groups： Control （CON, saline vehicle）, SB 203580 （SB, a p38 MAPK inhibitor） , R_PC, ischemia preconditioning （IPC）, SB ＋ RPC, SB ＋ IPC, RPC ＋ SB and IPC ＋ SB. Infarct size （IS）, a percentage of the area at risk （AAR） , was determined by triphenyltetrazolium（ TTC ） staining. Tissue simple were processed from the entire AAR of left ventricle for the determination of p38 MAPK protein expression （5 hearts/group）. The bands representing the proteins were visualised using an enhanced Chemiluminescence detection system. Results IS/AAR was reduced by IPC or RPC, compare to CON. SB administered prior to PC abolished effect of IS/ AAR reduction of IPC but RPC Treatment of SB prior to sustained ischemia diminished both protective effect of RPC and IPC on IS/ AAR. In IPC group, phospho-p38 MAPK protein increased significantly within 5 min ischemia and remained elevating at 30 rain reperfusion, while phospho-p38 MAPK protein in RPC increased significantly at 30 min reperfusion only. Conclusion The activation of p38 MAPK acts as a mediator of RPC, while it may have trigger and mediator effects in IPC.

关 键 词：心脏缺血再灌注损伤 MAPK家族 损伤保护机制 缺血预处理 瑞芬太尼 p38 丝裂原活化蛋白激酶 心脏保护作用 

分 类 号：R614[医药卫生—麻醉学]