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目的观察17β-雌二醇(E2)在大鼠心肌缺血再灌注损伤(myocardial ischemia-reperfusion injury,MIRI)过程中对肝细胞生长因子(hepatocyte growth factor,HGF)mRNA的表达影响并探讨其与细胞凋亡的关系。方法雄性SD大鼠40只,利用随机数字表将其分为缺血再灌注组(即对照组)、17β-雌二醇作用后的缺血再灌注组(即E2作用组),每组20只。结扎大鼠冠状动脉左前降支20min,再灌注30min,造成心肌缺血再灌注损伤模型,观察17β-雌二醇对心肌HGF表达的影响,同时测定心肌细胞的凋亡。结果心肌缺血20min及再灌注30min时,E2作用组HGFmRNA表达均较对照组相应时点显著增高(P<0.05)。TUNEL法检测E2作用组再灌注30min单位面积内心肌细胞凋亡较对照组明显减低(P<0.05);同时流式细胞仪检测结果显示,E2作用组亦显著低于对照组(P<0.05)。对照组再灌注30min及E2作用组再灌注30min的HGFmRNA表达变化与相应时间点的心肌细胞凋亡变化成负相关。结论17β-雌二醇在大鼠心肌缺血再灌注损伤(MIRI)过程中可提高HGF的表达,来发挥抗凋亡作用。
Objective To investigate the effect of 17β-estradiol (E2) on the mRNA expression of hepatocyte growth factor (HGF) during the myocardial ischemia-reperfusion injury (MIRI) The relationship between apoptosis. Methods Forty male Sprague-Dawley rats were randomly divided into ischemia-reperfusion group (control group) and ischemia-reperfusion group (E2-treated group) with 17β-estradiol only. The left anterior descending branch of coronary artery was ligated for 20min and then reperfused for 30min. The model of myocardial ischemia-reperfusion injury was established. The effect of 17β-estradiol on the expression of HGF in myocardium was observed, and the apoptosis of cardiomyocytes was also measured. Results Compared with the control group, the expression of HGF mRNA in E2-treated group was significantly increased at 20 min after myocardial ischemia and 30 min after reperfusion (P <0.05). The apoptosis of cardiomyocytes in the E2 treated group was significantly lower than that in the control group (P <0.05) by the TUNEL assay. The results of flow cytometry showed that the E2-treated group was significantly lower than that of the control group (P <0.05) . The changes of HGF mRNA expression in control group at 30 min after reperfusion and at 30 min after reperfusion were negatively correlated with the changes of myocardial apoptosis at corresponding time points. Conclusion 17β-estradiol can enhance the expression of HGF during myocardial ischemia-reperfusion injury (MIRI) to exert anti-apoptotic effects.