[Effects of ischemia postconditioning on ischemia-reperfusion injury and reperfusion injury salvage kinase signal transduction pathways in isolated mouse hearts].
OBJECTIVE
To explore the effects of ischemia postconditioning (IPC) on ischemia-reperfusion (I/R) injury and associated reperfusion injury salvage kinase (RISK) signal transduction pathways changes in isolated mouse hearts.


METHODS
Langendorff 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 min 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 reperfusion after 30 min ischemia and at one minute after reperfusion; (5) IPC + ERK1/2 inhibitor PD98059 (10(-5) mol/L for 15 min); (6) I/R + ERK1/2 inhibitor PD98059 (10(-5) mol/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 cardioprotective 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.
Zhang
Jian-fa
JF
Department of Cardiology of the First Affiliated Hospital, Xin Jiang Medical University, Urumqi 830054, China.
Ma
Yi-tong
YT
Yang
Yi-ning
YN
Gao
Xiao-ming
XM
Liu
Fen
F
Chen
Bang-dang
BD
Li
Xiao-mei
XM
Xiang
Yang
Y
D000818:Animals; D004195:Disease Models, Animal; D019157:Ischemic Preconditioning, Myocardial; D051379:Mice; D008810:Mice, Inbred C57BL; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism*; D017202:Myocardial Ischemia / Q000378:metabolism* / Q000628:therapy; D015428:Myocardial Reperfusion Injury / Q000378:metabolism* / Q000628:therapy; D015398:Signal Transduction
D020928:Mitogen-Activated Protein Kinases