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ASSA13-03-23 Effects Caused by Postconditioning of Mouse Heart Suffering from Reperfusion Injury and Mechanisms Induced by Reperfusion Injury Salvage Kinase
  1. Yang Yining,
  2. Ma Yitong,
  3. Liu Fen,
  4. Chen Bangdang,
  5. Li Xiaomei,
  6. Huang Ying
  1. Department of Cardiology of the First Affiliated Hospital, Xin Jiang Medical University, Urumqi 830011, China


Objective Explore cardioprotective mechanisms induced by reperfusion injury salvage kinase (ERK1/2) signal transduction pathways changes in isolated mouse hearts.

Methods Established Langendorff perfused mouse heart model, 96 C57BL mouse hearts were divided to 4 groups: 1) I/R control: 30 min global ischemia and 2 h reperfusion; 2) IPC:IPC with 3 episodes of 10 s of ischemia and 10 s reperfusion after 30 min ischemia and before 2 h reperfusion; 3) IPC+ERK1/2 inhibitor PD98059 (10–5 mol/L for 15 min); 4) I/R+ERK1/2 inhibitor PD98059 (10–5 mol/L for 15 min). The effects of IPC on Ischemic size, myocardial cell apoptosis index, phospho-protein kinase (P-ERK1/2) and phospho-protein kinase B(P-Akt) were measured. Expressions of apoptosis related proteins, including Bax, Bcl-2 and Cyt.C, in cytosolic and membrane fraction were detected by Western blot.

Results Following 180min reperfusion, infarct size was significantly reduced in postconditioning group (32.8 ± 3. 8)% compared with I/R group hearts [(48.1 ± 4.8)%, P < 0.05], and equally improved myocardial function compared with I/R group (all P < 0.05). Compared with ischemia reperfusion group, ischemic postconditioning group markedly decreased apoptotic index (AI)(P < 0.05), increased the mRNA expression of Bcl-2 gene (P < 0.05), the ratio of Bcl-2 to Bax was incidentally up-regulated (P < 0.05). Although IPC did not induce changes in the level of Bcl-2 expression in cytosolic fraction compared with I/R groups, the expression of Bcl-2 inmembrane fraction was up regulatedin IPC group compared with I/R group. The increase in the lease of mitochondrial Cyt.C into cytosol induced by I/R was significantly reduced by IPC. The histopathological changes in mitochondria and myocardium destroyed by ischemia repefusion were alleviated markedly by ischemic postconditioning. IPC significantly increased myocardial ERK1/2 phosphorylation, PD98059 inhibited the phosphorylation of ERK1/2 and abolished the cardioprotective effects induced by IPC.

Conclusions Postconditioning plays a pivotal role in reducing myocardial infarct size after ischemia/reperfusion injury. IPC right before reperfusion but not after reperfusion attenuated I/R injury of isolated mouse hearts via the upstream target, ERK1/2-MAPK signal transduction pathway which mediated the expression of Bcl-2/Bax and the release of mitochondrial Cyt.C.

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