title: [Effects of ischemia postconditioning on ischemia-reperfusion injury and reperfusion injury salvage kinase signal transduction pathways in isolated mouse hearts].
abstract: 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.
authors.affiliation: Department of Cardiology of the First Affiliated Hospital, Xin Jiang Medical University, Urumqi 830054, China.
authors.forename: Jian-fa
authors.initials: JF
authors.lastname: Zhang
authors.forename: Yi-tong
authors.initials: YT
authors.lastname: Ma
authors.forename: Yi-ning
authors.initials: YN
authors.lastname: Yang
authors.forename: Xiao-ming
authors.initials: XM
authors.lastname: Gao
authors.forename: Fen
authors.initials: F
authors.lastname: Liu
authors.forename: Bang-dang
authors.initials: BD
authors.lastname: Chen
authors.forename: Xiao-mei
authors.initials: XM
authors.lastname: Li
authors.forename: Yang
authors.initials: Y
authors.lastname: Xiang
mesh_terms: 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
chemical_list: D020928:Mitogen-Activated Protein Kinases