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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 investigate the protective effects of iIPC on myocardium and the role of myocardial mitochondrial uncoupling protein-2 (UCP2) in protection of iIPC myocardium. Methods: The rat model of iIPC was established by ligation of the superior mesenteric artery (SMA). Myocardial ischemia-reperfusion (IR) was performed on the model rats to evaluate the degree of myocardial injury. The myocardial tissue was analyzed by RT- The relative content of UCP2. Myocardial ischemia-reperfusion rats without ligating SMA were the IR control group and the sham-operated rats were blank control group. Results: ① The ultrastructural damage of myocardial cells in IR control group was significantly more than that of blank control group, but iIPC group was lighter than IR control group at 0 and 24 h after iIPC. ②Compared with the IR control group, UCP2 mRNA levels in myocardium were significantly increased at 0, 6, 12, 24 and 48 h in iIPC group (P <0.01); UCP2 mRNA level showed biphasic changes in iIPC group, UCP2 level at 0 h The highest, 6 h after the decline, 24 h rise again, then gradually decline. CONCLUSION: iIPC can protect myocardium IR. The expression of UCP2 in preconditioned rat myocardium is significantly increased, suggesting that UCP2 might be involved in the protective effect of iIPC on myocardium.