Effects of ischemia postconditioning on isehemia-reperfusion injury and reperfusion injury salvage kinase signal transduction pathways in isolated mouse hearts
10.3321/j.issn:0253-3758.2008.02.015
- VernacularTitle:再灌注损伤抢救激酶对小鼠缺血后适应心肌再灌注损伤中的减轻作用
- Author:
Jian-Fa ZHANG
1
;
Yi-Tong MA
;
Yi-Ning YANG
;
Xiao-Ming GAO
;
Fen LIU
;
Bang-Dang CHEN
;
Xiao-Mei LI
;
Yang XIANG
Author Information
1. 新疆医科大学附属第一医院
- Keywords:
Myocardial ischemia;
Reperfusion injury;
Mitogen-activated protein kinases;
Ischemia postconditioning
- From:
Chinese Journal of Cardiology
2008;36(2):161-166
- CountryChina
- Language:Chinese
-
Abstract:
Objeetive To explore the effects of ischemia postconditioning(IPC)on ischemia-reperfusion(I/R)injury and associated reperfusion injury salvage kinase(RISK)signal transduction palthways changes in isolated mouse hearts.Methods Langendofff perfused C57/BL mouse hearts were divided to 6 groups:(1)control:30 min global ischemia and 2 h reperfusion(I/R);(2)IPC with 3 episodes,IPC with 3 episodes of 10 s of ischemia and 10 s reperfusion after 30 rain ischemia and before 2 h reperfusion:(3)IPC with 6 episodes,IPC with six episodes of 10 s of ischemia and 10 s reperfusion after 30 min ischemia and before 2 h reperfusion:(4)delayed IPC,IPC with 3 episodes of 10 s of ischemia and 10 s repeflusion after 30 min ischemia and at one minute after reperfusion;(5)IPC+ERK1/2 inhibitor PD98059(10-5mol/L for 15 min);(6)L/R+ERK1/2 inhibitor PD98059(10-5mol/L for 15 min).The effects of IPC on hemodynamics,coronary artery flow,creatine kinase(CK)and lactate dehydrogenase (LDH)release,myocardial SOD,MDA,phospho-protein kinase(P-ERK1/2)and phospho-protein kinase B(P-Akt)as well as myocardial infarction size were measured.Results IPC with 3 episodes and IPC with 6 episodes significantly and equally improved myocardial function,increased myocardial SOD,reduced CK and LDH release and myocardial infarction size compared with IR group(all P＜0.01)while these parameters were similar between I/R hearts and delayed IPC hearts.IPC significantly increased myocardial ERK1/2 phosphorylation.PD98059 inhibited the phosphorylation of ERK1/2 and abolished the cardioDrotective effects induced by IPC.Conclusions IPC obviously attenuated I/R injury in isolated mouse hearts,the cardioprotection of IPC was not enhanced because of increasing of IPC episodes and disappeared in delayed IPC.The cardioprotective effects of IPC were mediated through ERK1/2-MAPK signal transduction pathway.
