Li Chun-Mei, Shen Shu-Wen, Wang Tao, Zhang Xing-Hua
Department of Cardiology, Shandong Provincial Hospital Affiliated to Shandong University Jinan 250021, Shandong, China.
Department of Cardiology, Shandong Traffic Hospital Jinan 250031, Shandong, China.
Int J Clin Exp Med. 2015 Sep 15;8(9):15801-7. eCollection 2015.
To investigate whether myocardial ischemic post-conditioning attenuates ischemia reperfusion injury via PTEN/Akt signal pathway.
Forty-five male Sprague-Dawley rats were randomly divided into three groups: Sham, Ischemia reperfusion (I/R) and Ischemic post-conditioning (IPost) group. After the experiment finished, myocardial infarction area was examined. Serum creatine phosphokinase and lactate dehydrogenase activity were detected at baseline and the end of reperfusion. The protein levels of PTEN, Akt, p-Akt, Bax and Bcl-2 were measured by Western blot method.
Myocardial infarct size was significantly reduced in IPost as compared to I/R. Results were confirmed by serum creatine phosphokinase and lactate dehydrogenase activity. In addition, PTEN and Bax protein expression were inhibited and the p-Akt and bcl-2 protein expression were enhanced in IPost compared with I/R (P < 0.05). At the same time, the ratio of Bax and Bcl-2 was decreased in IPost (P < 0.05). However, ischemic post conditioning did not affect the total Akt level (P > 0.05).
We confirmed that ischemic post-conditioning protects the heart against reperfusion injury. It is important that we demonstrated that the cardioprotective effect of ischemic post-conditioning was involved in the inhibition of PTEN, activation of the PI3K/Akt pathway and reduction of the cardiomyocyte apoptosis.
探讨心肌缺血后处理是否通过PTEN/Akt信号通路减轻缺血再灌注损伤。
45只雄性Sprague-Dawley大鼠随机分为三组:假手术组、缺血再灌注(I/R)组和缺血后处理(IPost)组。实验结束后,检测心肌梗死面积。在基线和再灌注结束时检测血清肌酸磷酸激酶和乳酸脱氢酶活性。采用蛋白质印迹法检测PTEN、Akt、p-Akt、Bax和Bcl-2的蛋白水平。
与I/R组相比,IPost组心肌梗死面积显著减小。血清肌酸磷酸激酶和乳酸脱氢酶活性的结果证实了这一点。此外,与I/R组相比,IPost组PTEN和Bax蛋白表达受到抑制,p-Akt和bcl-2蛋白表达增强(P<0.05)。同时,IPost组Bax与Bcl-2的比值降低(P<0.05)。然而,缺血后处理不影响Akt的总水平(P>0.05)。
我们证实缺血后处理可保护心脏免受再灌注损伤。重要的是,我们证明了缺血后处理的心脏保护作用与抑制PTEN、激活PI3K/Akt通路以及减少心肌细胞凋亡有关。