Department of Cardiology, Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, China.
Biomed Res Int. 2016;2016:9349437. doi: 10.1155/2016/9349437. Epub 2016 Dec 20.
We investigated the cardioprotective effect of renal ischemic postconditioning (RI-PostC) and its mechanisms in a rabbit model. Rabbits underwent 60 min of left anterior descending coronary artery occlusion (LADO) and 6 h of reperfusion. The ischemia-reperfusion (IR) group underwent LADO and reperfusion only. In the RI-PostC group, the left renal artery underwent 3 cycles of occlusion for 30 seconds and release for 30 seconds, before the coronary artery was reperfused. In the RI-PostC + GF109203X group, the rabbits received 0.05 mg/kg GF109203X (protein kinase C inhibitor) intravenously for 10 min followed by RI-PostC. Light microscopy and electron microscopy demonstrated that the RI-PostC group showed less pronounced changes, a smaller infarct region, and less apoptosis than the other two groups. Bcl-2 and Bax protein expression did not differ between the IR and RI-PostC + GF109203X groups. However, in the RI-PostC group, Bcl-2 protein expression was significantly higher and Bax protein expression was significantly lower than in the other two groups ( < 0.05). Changes in heart rate and mean arterial pressure were also smaller in the RI-PostC group than in the other two groups. These results indicate that RI-PostC can ameliorate myocardial ischemia-reperfusion injury and increase the Bcl-2/Bax ratio through a mechanism involving protein kinase C.
我们在兔模型中研究了肾缺血后处理（RI-PostC）的心脏保护作用及其机制。兔经历了 60 分钟的左前降支冠状动脉闭塞（LADO）和 6 小时的再灌注。缺血再灌注（IR）组仅进行 LADO 和再灌注。在 RI-PostC 组中，左肾动脉经历了 3 个循环的闭塞 30 秒和释放 30 秒，然后再进行冠状动脉再灌注。在 RI-PostC+GF109203X 组中，兔接受了 0.05mg/kg GF109203X（蛋白激酶 C 抑制剂）静脉内注射 10 分钟，然后进行 RI-PostC。光镜和电镜观察表明，与其他两组相比，RI-PostC 组的变化不明显，梗死区域较小，凋亡较少。Bcl-2 和 Bax 蛋白表达在 IR 和 RI-PostC+GF109203X 组之间没有差异。然而，在 RI-PostC 组中，Bcl-2 蛋白表达明显高于其他两组，Bax 蛋白表达明显低于其他两组（<0.05）。RI-PostC 组的心率和平均动脉压变化也小于其他两组。这些结果表明，RI-PostC 可以通过涉及蛋白激酶 C 的机制改善心肌缺血再灌注损伤并增加 Bcl-2/Bax 比值。
