摘要
目的探讨血红素氧合酶-1(HO-1)对大鼠心肌缺血/再灌注损伤的保护效应及作用机制。方法采用HO-1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心肌缺血/再灌注损伤模型,观察大鼠再灌注后I/R左心室心肌超微结构变化;检测HO-1蛋白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蛋白表达上调。HO-1蛋白表达上调可以减少缺血/再灌注后心肌细胞坏死,提高心肌组织中SOD含量,并降低MDA含量。结论CoPP诱导的HO-1过表达可以抑制心肌缺血/再灌注损伤后细胞坏死,从而减轻心肌再灌注损伤,抗氧自由基是其机制之一。
Objective To investigate the protective effects of HO-1 on myocardial ischemia/reperfusion injury of rats in vivo,and explore the possible mechanism. Methods Rat myocardial ischemia/reperfusion injury model was established. The expression of HO-1 protein was detected, the vitality of SOD and the quantity of MDA was detected in rat myocardial ischemia/reperfusion injury model treated with Cobalt protoporphyrin（HO-1 inducer） or Zinc protoporphyrin（HO-1 inhibitor）. Results Pretreatment of CoPP before reperfusion could up-regulate the expression of HO-1 and enhance the vitality of SOD, and decrease the quantity of MDA, subsequently reduce the incidence of necrosis atter myocardial reperfusion. Conclusion The up-regulation of HO ] expression in- duced by CoPP can inhibit the necrosis of the myocardial cells and subsequently alleviate the myocardial ischemia/ reperfusion inju- ry,one which of its main mechanisms may he related with the anti-oxygen free radicals.
出处
《重庆医学》
CAS
CSCD
北大核心
2009年第11期1384-1385,F0003,共3页
Chongqing medicine
关键词
血红素氧合酶-1
心肌缺血/再灌注损伤
保护作用
抗氧自由基
heine oxygenase-1
myocardial ischemic reperfusion injury
protective effects
anti oxygen free radicals
