Acute Cardioprotective Effect of 17b-estradiol on a Rabbit Model of Myocardial Ischemia/Reperfusion Injury

Objective To investigate the acute cardioprotective effect of 17b-estradiol(17b-E2) against severe myocardial ischemia/reperfusion(I/R) injury in rabbits and the mechanism of the effect.Methods We established the model of myocardial I/R in vivo by occluding the left anterior descending coronary artery of the rabbits(who underwent coronary occlusion for 40 minutes followed by 3 hours of reperfusion).Twenty-four New Zealand white male rabbits were randomly divided into two groups with 12 in each group. Before coronary occlusion,1 ml of ethanol or 17b-E2 at 10 μg/kg was administered intravenously to the rabbits in the control group and the experimental group respectively.The serum levels of tumor necrosis factor-α(TNF-α) and interleukin-6(IL-6) were measured by enzyme-linked immunosorbent assay(ELISA) at the following time points: before occlusion,40 minutes after occlusion,1 hour,2 hours and 3 hours after reperfusion.Activation of p38 mitogen activated protein kinase(MAPK) was determined by Western blotting analysis,and apoptosis of cardiocytes was identified by terminal deoxynucleotidlyl transferase mediated deoxyuridine-biotin dUTP Nick End Labeline(TdT)-mediated dNTP nick end labeling(TUNEL) staining.Results During myocardial ischemia,TNF-α decreased significantly in the experimental group compared with the control group(F=0.007,P=0.001),while there was no difference in IL-6 between the two groups(F=0.616,P=0.095).During the process of reperfusion,the levels of TNF-α and IL-6 in the experimental group were significantly lower than those in the control group(P0.01).Besides,the activation of p38 MAPK and apoptotic index for the experimental group were also lower(45.07%±2.73% vs. 61.25%±2.41%,t=-15.398,P=0.000;11.21%±3.85% vs.22.02%±4.49%,t=-6.332,P=0.000).Conclusion The cardioprotective effect of 17b-E2 against myocardial I/R may be attributed to its anti-inflammatory and anti-apoptotic properties,which is probably associated with the inhibition of 17b-E2 on p38MAPK activity.