血红素氧合酶-1对大鼠心肌缺血-再灌注损伤的保护作用研究

目的探讨血红素氧合酶-1(HO-1)对大鼠心肌缺血-再灌注损伤的效果及作用机制。方法采用HO-1的诱导剂钴原卟啉(CoPP)和抑制剂锌原卟啉(ZnPP)分别进行干预处理后,建立大鼠的心肌缺血-再灌注损伤模型,观察大鼠再灌注后心肌形态变化;检测血红素氧合酶-1基因在大鼠心肌的表达情况;测定大鼠左心室心肌组织超氧化物歧化酶(SOD)活性及丙二醛(MDA)含量。结果再灌注前使用CoPP进行预处理,可以诱导HO-1蛋白的表达上调。HO-1蛋白表达上调可以减少缺血-再灌注后的心肌细胞坏死,提高心肌组织中SOD含量并降低MDA的含量。结论CoPP诱导的HO-1过表达可以抑制心肌缺血-再灌注损伤后的细胞坏死,从而减轻心肌的再灌注损伤,其主要机制与抗氧自由基有关。

The Protective Effect of HO-1 on Myocardial Ischemia/Reperfusion Injury in Rats

Objective To investigate the protective effects of heme oxygenase (HO)-1 on myocardial ischemia/reperfusion injury of rats in vivo, and explore the possible mechanism. Methods Rat myocardial ischemia/reperfusion injury models were established. The expression of HO-1 mRNA was detected by RT-PCR. The vitality of SOD and the quantity of MDA were detected in rat myocardial ischemia/reperfusion injury models treated with HO-1 inducer cobalt protoporphyrin (CoPP) or zinc protoporphyrin (HO-1 inhibitor).Results Pretreatment of CoPP before reperfusion up-regulated the expression of HO-1, enhanced the vitality of SOD, decreased the quantity of MDA, and subsequently reduced the incidence of necrosis atter myocardial reperfusion. Conclusion The up-regulation of HO-1 expression induced by CoPP can inhibit the necrosis of the myocardial cells and subsequently alleviate the myocardial ischemia/reperfusion injury. One of its main mechanisms may be related with anti-oxygen free radicals.