超氧化物歧化酶清除自由基对心肌缺血再灌注损伤的保护作用及其机制

The research on the mechanism of superoxide dismutase remove free radicals play a protective effect in myocardial ischemia reperfusion injury

目的 建立小鼠心脏缺血再灌注损伤模型,分别给予两种超氧化物歧化酶（SOD）类似物进行干预治疗,观察心肌组织缺血再灌注以及缺血再灌注后心脏的功能状态.方法 建立小鼠心脏缺血再灌注模型,分别在灌注前5 min给予小鼠SOD类似物及磷酸盐缓冲液（PBS）.通过Evans蓝和氯化三苯基四氮唑（TTC）双染色测定梗死心肌面积,激光多普勒测定心肌缺血再灌注后心肌血流量和心功能变化,观察小鼠缺血再灌注心脏损伤变化.结果 采用小鼠心脏冠状动脉左前降支结扎,成功构建小鼠心肌缺血再灌注损伤模型,模型成功率达96％.采用SOD类似物在缺血再灌注前进行干预,可明显减少小鼠心脏再灌注过程中心功能损伤,其中心肌梗死面积由65％下降至37％,平均动脉血压（MABP）平均变化率由33.3％降低为18.9％,差异均有统计学意义（P＜0.05）.结论 氧自由基分子是心肌缺血再灌注损伤的关键分子,SOD类似物可以通过清除氧自由基来发挥对心肌缺血再灌注损伤的保护作用.

Objective In this study,we establishment the mouse cardiac ischemia repeffusion model,given two superoxide dismutase （SOD） analogues,in order to observe cardiac functions of myocardial ischemia reperfusion and ischemia reperfusion.Methods Establishment of mouse cardiac ischemia reperfusion model.Mice were given SOD analogues and phosphate buffer （PBS） in 5 min respectively before perfusion.By Evans blue and TTC staining determination of myocardial infarct area,laser Dopplermeasurement and changes of myocardial blood flow perfusion and heart function of myocardial ischemia,ischemia repeffusion injury of heart were observed changes.Results Mouse heart left anterior descending coronary artery ligation in mice with myocardial ischemia repeffusion injury model was constructed successfully,the success rate of the model 96%.Using SOD analogs to intervene before ischemia-reperfusion can obviously reduce the mouse cardiac reperfusioninjury center function,the area of myocardial infarction decreased from 65% to 37%,the average change in mean arterial blood pressure （MABP） rate reduced from 33.3% to 18.9%,the differences were statistically significant （P 〈 0.05）.Conclusion Oxygen free radicals is the key molecule of myocardial ischemia and reperfusion injury,SOD mimic can play a protective effect on myocardial ischemia repeffusion injury by scavenging oxygen free radicals.