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H2S restores the cardioprotection from ischemic post-conditioning in isolated aged rat hearts

机译:H2S可恢复离体老年大鼠心脏缺血后的心脏保护作用

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This study explored the mechanisms underlying the recovery of myocardial protection from ischemic post-conditioning (PC) by exogenous hydrogen sulfide (H2S) in aged rat hearts. We observed that ischemia/reperfusion (I/R) inhibited the phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) and promoted phosphorylation of p38 MAPK and c-Jun N-terminal kinase (JNK) in both young hearts and aged hearts. PC up-regulated ERK1/2 phosphorylations and down-regulated p38 MAPK and JNK phosphorylations. Exogenous H2S further enhanced the role of PC in the young hearts. In the aged hearts, PC failed to affect all these 3 MAPK members, while co-treatment with exogenous H2S-induced ERK1/2 and reduced p38 MAPK and JNK phosphorylations. These results suggest that exogenous H2S recovers PC-induced cardioprotection via MAPK pathway in the aged hearts.
机译:这项研究探讨了外源性硫化氢(H2S)在老年大鼠心脏中从缺血性后处理(PC)恢复心肌保护的潜在机制。我们观察到缺血/再灌注(I / R)抑制了幼鼠和幼鼠心脏中细胞外信号调节激酶1/2(ERK1 / 2)的磷酸化,并促进了p38 MAPK和c-Jun N端激酶(JNK)的磷酸化。年迈的心。 PC上调ERK1 / 2磷酸化和下调p38 MAPK和JNK磷酸化。外源性H2S进一步增强了PC在年轻心脏中的作用。在老年心脏中,PC不能影响所有这3个MAPK成员,而与外源性H2S诱导的ERK1 / 2共同治疗并降低p38 MAPK和JNK磷酸化。这些结果表明,外源性H2S通过MAPK途径恢复了老年心脏中PC诱导的心脏保护作用。

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