کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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6254459 | 1288445 | 2012 | 8 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: CardiothoracicSufentanil postconditioning protects the myocardium from ischemia-reperfusion via PI3K/Akt-GSK-3β pathway CardiothoracicSufentanil postconditioning protects the myocardium from ischemia-reperfusion via PI3K/Akt-GSK-3β pathway](/preview/png/6254459.png)
BackgroundPrevious studies have shown that opioid postconditioning reduces apoptosis through antiapoptotic signaling. The present study evaluated whether sufentanil could induce cardioprotection after ischemia-reperfusion (I/R) and whether the PI3K/Akt-GSK-3β pathway modulates antiapoptotic proteins in sufentanil postconditioning.MethodsWe subjected male Sprague-Dawley rats to 30 min of myocardial ischemia and 2 h of reperfusion. We randomized rats into seven groups: sham, I/R, sufentanil postconditioning (I/R+sufen), sham plus sufentanil (sham+sufen), sham plus 15 μg·kgâ1 intravenous wortmannin (PI3K inhibitor), I/R plus wortmannin, and sufentanil plus wortmannin. We induced sufentanil postconditioning with 3 μg·kgâ1 sufentanil for 3 min in the beginning of reperfusion after 30 min ischemia. We assessed hemodynamics, myocardial infarct size, number of apoptotic cardiomyocytes, total Akt and GSK-3β, phosphorylated Akt and GSK-3β, caspase-3, Bax, and Bcl-2 protein expression.ResultsThe I/R+sufen group had significantly reduced infarct size compared with the I/R group (23.3% ± 9.0% versus 50.1% ± 7.4%; P < 0.05). The apoptotic index of cardiomyocytes was significantly reduced with sufentanil treatment (20.0% ± 3.5%) compared with the I/R group (47.0% ± 6.3%; P < 0.05). The I/R+sufen group reduced the expression of protein-cleaved caspase-3 and Bax, and increased Bcl-2, phosphorylated Akt, and GSK3β compared with the I/R group. Wortmannin eliminated the cardioprotection produced with sufentanil treatment.ConclusionsSufentanil postconditioning can induce myocardial protection by activating the PI3K/Akt-GSK-3β pathway and modulating Bax and Bcl-2 expression.
Journal: Journal of Surgical Research - Volume 178, Issue 2, December 2012, Pages 563-570