雌激素对大鼠缺血心肌的保护作用

目的]探讨雌激素在大鼠心肌缺血过程中的保护作用。方法]将30只大鼠随机分为3组（每组10只）,⑴假手术组（S组）：对冠脉只穿线不结扎;⑵单纯缺血组（I组）：冠脉结扎;⑶17β-雌二醇（E2）干预后的缺血组（E2组）：利用1 mL E2（5μmol/L）干预1周,然后行冠脉结扎。除假手术组外,其余两组均通过结扎SD大鼠冠状动脉左前降支制备缺血20 min的大鼠心肌缺血损伤模型,检测心肌组织超氧化物歧化酶（SOD）、丙二醛（MDA）水平,测定心肌细胞凋亡情况。结果]①SOD值在S组、I组与E2组分别为（105.311±3.472）U/mL、（79.931±3.116）U/mL和（94.396±2.219）U/mL,其中后两组明显低于S组（P〈0.05）;MDA值在S组、I组与E2组分别为（18.842±1.166）μmol/g、（25.074±0.654）μmol/g和（19.745±0.917）μmol/g,I组较S组明显增高（P〈0.01）;②与I组SOD,MDA相比,E2组SOD活性及MDA值差异均有显著性意义（P〈0.05）;③E2组凋亡指数（34.67±8.85）低于I组（49.00±8.07）,两者间差异存在显著性意义（P〈0.05）。结论]E2对心肌缺血具有保护作用,其机制可能是通过抗氧自由基损伤及抗心肌细胞凋亡发挥作用。

Protective effect of estrogen on cardiac myocytes during ischemia process

Objective] To study the protective effect of estrogen on rat heart during ischemia injury.Methods] The 30 rats were randomly assigned into three groups(10 rats/each group): the sham group(S group),ischemia group(I group) and estrogen intervention group(E2 group).Rat heart ischemia was performed by ligating the left anterior descending coronary artery for 20 min,the sham group exposed the heart but without ligation.E2(5 μmol/L) was abdominaly injected 1 week before heart ischemia in E2 group.Results] ①The values of superoxide dismutase(SOD) activity of the S group,I group and E2 group were(105.311±3.472) U/mL,(79.931±3.116) U/mL and(94.396±2.219) U/mL respectively.Comparing with the S group,they all decreased significantly(P<0.05);Malondialdehyde(MDA) contents of the S group,I group and E2 group were(18.842±1.166) μmol/g,(25.074±0.654) μmol/g and(19.745±0.917) μmol/g respectively.It was significant increasing(P<0.01) in the I group comparing with the S group;②Comparing with the I group,the values of SOD(94.396±2.219) U/mL and MDA(19.745±0.917) μmol/g in E2 group were changed significantly(P<0.05);③Apoptosis index of E2 group(34.67±8.85) was significantly lower than I group(49.00±8.07)(P<0.05).Conclusions] E2 has the protective effect on rat heart against ischemia injury,the mainly mechanism maybe through anti oxygen free radicals and then reducing apoptosis of cardiac myocytes.