地塞米松对I/R心肌梗死面积及抗氧自由基酶的影响

The Effect of Dexamethasone on Sizes of Infarction and Contents of MDA,SOD,CAT,GSH-Px in Rat Hearts Induced by Ischemia/reperfusion

目的:探讨地塞米松预处理对大鼠缺血-再灌注(I/R)心肌梗死面积的影响及机制。方法:SD大鼠随机分成地塞米松组、对照组,分别予地塞米松和生理盐水预处理。预处理后构建Langendorff离体心脏I/R动物模型,缺血30 min后再灌注60 min,测定心肌丙二醛(MDA)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化酶(GSH-Px)水平;TTC法测定心肌梗死面积;观察心肌超微结构变化。结果:与对照组相比,地塞米松组MDA水平显著降低(P<0.01),SOD、CAT、GSH-Px水平升高(P<0.05);心肌梗死面积明显缩小(P<0.01)。结论:地塞米松可减轻缺血再灌注后心肌梗死面积及心肌超微结构的损伤,其机制可能通过升高心肌组织抗氧自由基酶的水平、抑制脂质过氧化反应有关。

Objective： To explore the effect of dexamethasone （DEX） preconditioning on the myocardial infarction sizes caused by ischemia/reperfusion （I/R） and its mechanism. Methods： Forty- eight Sprague-Dawley rats were divided randomly into DEX and control （CON） groups, of which the rats were pretreaded with DEX （ DEX group） or sodium chloride （ CON group） before their hearts were separated for Langendorff perfusion and ischemia/reperfusion. The 30-minute ischemia was caused by triphenyhetrazolium chloride （TTC） and followed by 60-minute reperfusion. The myocardial infarction sizes were measured and the myocardial ultrastructures were examined afterwards. The reperfusion caused myocardial injury, malonaldehyole （ MDA）, superoxide dismutase （ SOD）, catalase （ CAT）, and glutathione peroxidase （GSH-Px） were detected. Results： Compared with control group, the MDA was significantly lower （P 〈 0.01 ） and the SOD, CAT, GSH-Px were significantly higher in group DEX （P 〈0.05） ; The sizes of infarction were reduced significantly （P 〈0.01 ）. Conclusions： Dexamethasone can reduce the myocardial infarction sizes and the injury of myocardial ultrastructure during I/R. The mechanism might be the enhancement of myocardial antioxidase activity to inhibit lipid peroxidation.