缺血后处理对心肌缺血/再灌注大鼠血红素加氧酶-1表达的影响

目的:探讨缺血后处理对心肌缺血/再灌注大鼠血红素加氧酶-1(HO-1)表达的影响。方法:56只雄性SD大鼠随机分为4组:假手术组(Sham组)(n=8)、缺血再灌注组(I/R组)(n=16)、缺血后处理组(IPo组)(n=16)和血红素加氧酶抑制剂锌原卟啉组(ZnPP组)(n=16)。采用结扎心脏左冠状动脉前降支30 min,再灌注2 h制备心肌缺血再灌注损伤模型。IPo组在结扎心脏左冠状动脉前降支30 min,再灌注10 s,缺血10 s,重复3次后,完全恢复心肌血流。再灌注2 h后开胸,每组8只取心尖部缺血心肌,测定超氧化物歧化酶(SOD)活性、心肌组织中丙二醛(MDA)含量和心肌中HO-1蛋白表达。I/R组I、Po组和ZnPP组另取8只大鼠测定心梗面积。结果:与S组比较,I/R组缺血心肌中MDA含量增加,SOD活性降低(P<0.01),I/R组HO-1表达无统计学差异(P>0.05)。与I/R组比较,IPo组缺血心肌中MDA降低,SOD活性升高且心梗面积明显减小(P<0.01),HO-1蛋白表达显著增强(P<0.01)。与IPo组比较,ZnPP组MDA含量升高,SOD活性降低(P<0.01),HO-1表达明显减少(P<0.01)。结论:缺血后处理能减轻大鼠心肌缺血再灌注损伤,其机制与增强心肌抗氧化能力和增加血红素加氧酶(HO-1)的表达有关。

Effects of Ischemic Postconditioning on the Expression of HO-1 in the Myocardium with Ischemia and Reperfusion Injury in Rats

Objective: To investigate the effects of ischemic postconditioning on the expression of HO-1 in the myocardial ischemia and reperfusion injury in rats.Methods: Fifty-six male SD rats weighing 200-250 g were randomly divided into four groups: sham-operation group(sham)(n=8),ischemia and reperfusion group(I/R)(n=16),ischemic postconditioning group(IPo)(n=16) and inhibitor of HO-1 group(ZnPP)(n=16).The ischemia and reperfusion injury models in I/R was induced by occlusion of the left anterior descending branch of coronary artery(LAD) for 30 min followed by 2 h reperfusion.In IPo group,30 min ischemia was followed by three 10-second episodes of ischemia at 10-second intervals for reperfusion.At the end of 2 h reperfusion,the ischemic myocardial tissue was collected for the determination of MDA content,SOD activity,the expression of HO-1 and myocardial infarct size.Results: SOD activity was significantly lower whereas MDA content was significantly higher in I/R group than in S group(P<0.01).There was no significant difference in the expression of HO-1 between I/R group and sham group(P>0.05).MDA content and myocardial infarct size were significantly lower whereas SOD activity was significantly higher in IPo group than in I/R group,and the expression of HO-1 in IPo group was significantly stronger than that in I/R group(P<0.01).SOD activity and the expression of HO-1 were significantly lower whereas MDA content was significantly higher in ZnPP group than in I/R group(P<0.01).Conclusion: Ischemic postconditioning attenuates myocardium injury induced by I/R in rats.The underlying mechanism is related to the induction of HO-1 and enhancement of myocardium antioxidation.