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 ...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.展开更多
文摘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.
