解偶联蛋白-2在肠缺血预适应大鼠心肌中的表达

The expression of UCP2 in myocardium of rats with intestinal ischemic preconditioning

目的:探讨肠缺血预适应(iIPC)对心肌的保护作用以及心肌线粒体解偶联蛋白-2(UCP2)在iIPC心肌保护中的作用。方法:结扎肠系膜上动脉(SMA)制作iIPC大鼠动物模型,对模型大鼠进行心肌持续缺血-再灌注(IR),评价心肌损伤程度,并采用RT-PCR方法、计算机凝胶成像分析心肌UCP2的相对含量。以未结扎SMA的心肌持续缺血-再灌注大鼠为IR对照组,假手术大鼠为空白对照组。结果:①IR对照组大鼠心肌细胞超微结构损伤程度明显超过空白对照组,而iIPC组在iIPC后的0和24 h均轻于IR对照组。②与IR对照组大鼠心肌中UCP2mRNA水平比较,iIPC 0、6、12、24和48 h组均明显升高(P<0.01);iIPC后UCP2 mRNA水平呈双相变化,0 h心肌UCP2水平最高,6 h后下降,24 h再次升高,此后逐渐回落。结论:iIPC能对心肌IR产生保护作用,预适应大鼠心肌UCP2的表达明显升高,提示UCP2可能参与iIPC对心肌的保护作用。

Objective：To discuss the protective effect of intestinal ischemic preconditioning （iIPC） on the myocardium and the role of uncoupling protein 2 （UCP2） in myocardium with iIPC. Methods ： The animal model was built by superior mesenteric artery ligation of rats. Then they were subjected to a sustained coronary occlusion of 30 rain and reperfusion of 180 rain. We evaluated the degree of the myocardial damage and used RT-PCR method to check the relative content of UCP2 mRNA. The IR control group underwent the coronary occlusion/reperfusion with no intestinal ischemia and the blank group was sham-operated. Results：①Compared to the blank group, the IR control group showed much heavier damage in the ultramicro structure. And for the iIPC group, the damage in the ultramicro structure 0 h and 24 h after iIPC was lighter than that of the IR control group. ②Compared to the expression of the UCP2 mRNA in the myocardium of rats in the IR control group, the expressions of iIPC 0 h ,6 h, 12 h ,24 h,48 h groups increased substantially （P 〈 0.01 ）. And the development of the expression level can be divided into two phases. The level of UCP2 0 h after iIPC was the highest and decreased 6 h after iIPC. It increased again 24 h after the intestinal ischemia and dropped gradually after that. Conclusion： iIPC can protect myocardial cells from IR injury. UCP2 is involved in the mechanism of the cardioprotection induced by iIPC.