摘要
目的:探讨血红素加氧酶-1(HO-1)对心肌缺血再灌注损伤的保护作用及机制。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HO-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。
Objective To investigate the protective effect of heme oxygenase-1 （HO-1）on myocardial ischemia/ reperfusion injury in rats and its possible mechanism. Methods A rat model of myocardial ischemia/reperfusion injury was established by treating with HO-1 inducer cobalt protoporphyrin （CoPP）or inhibitor zinc protoporphyrin. Morphological changes of the myocardium were observed. Expression of HO-1 mRNA in the myocardial cells was detected by using RT-PCR. SOD activity and MDA content in the myocardial tissues of left ventricle were also detected. Result HO-1 expression was upregulated following pretreatment of CoPP before reperfusion, resulting in both an increase in SOD activity and a decrease in MDA content and thus in a reduction in death of the myocardial cells after ischemia/reperfusion injury, Conclusion The overexpression of HO-1 induced by CoPP can inhibit death of the myocardial cells and subsequently alleviate myocardial ischemia/reperfusion injury, whose major mechanism may be related with anti-oxygen free radicals.
出处
《实用医学杂志》
CAS
2008年第13期2211-2213,共3页
The Journal of Practical Medicine
关键词
心肌再灌注损伤
血红素氧化酶(脱环)
抗氧自由基
Myocardial reperfusion injury Heme oxygenase（decyclizing） Anti-oxygen free radicals
