Survivin: A novel player in insulin cardioprotection against myocardial ischemia/reperfusion injury
Survivin: A novel player in insulin cardioprotection against myocardial ischemia/reperfusion injury
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Survivin：胰岛素心脏保护作用中针对心肌缺血/再灌注损伤的新参与者。
DOI：
10.1016/j.yjmcc.2010.08.017
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发表时间：
2011-01-01
影响因子：
5
通讯作者：
Gao, Feng
中科院分区：
文献类型：
--
作者：
Si, Rui;Tao, Ling;Gao, Feng
胰岛素通过激活包括磷脂酰肌醇3-激酶(PI3K)-Akt通路在内的存活信号级联抑制缺血/再灌注诱导的心肌凋亡。然而，PI3K的下游机制尚不清楚。本研究旨在探讨survivin （SW）是否在胰岛素诱导的缺血/再灌注（I/R）心脏抗凋亡作用中起作用，如果起作用，进一步确定其信号机制。分离的成年大鼠心脏局部缺血30分钟，然后在再灌注开始时加胰岛素或不加胰岛素（10(-7)mol/L）再灌注。胰岛素再灌注抑制心肌凋亡，减少梗死面积，心肌SW表达显著上调(MI/R + Ins组5.9 +/- 0.3 vs. MI/R组2.1 +/- 0.1,p
Insulin inhibits ischemia/reperfusion-induced myocardial apoptosis through the activation of a survival signaling cascade including the phosphatidylinositol 3-kinase (PI3K)-Akt pathway. However, the downstream mechanism of PI3K remains elusive. This study is aimed at investigating whether survivin (SW) plays a role in the insulin-induced anti-apoptotic effect in the ischemic/reperfused (I/R) hearts, and if so, further determining the signaling mechanism involved. Isolated adult rat hearts were subjected to 30 min regional ischemia followed by reperfusion with or without insulin (10(-7) mol/L) at the onset of reperfusion. Reperfusion with insulin inhibited myocardial apoptosis and reduced infarct size, along with significantly up-regulated myocardial SW expression (5.9 +/- 0.3 Group MI/R + Ins vs. 2.1 +/- 0.1 Group MI/R, p