17β-Estradiol Nanoparticles Increase Endothelial Nitric Oxide Synthase Expression Through Akt Pathway in Rats with Myocardial Infarction

Abstract

17β-estradiol can effectively slow down progression of myocardial infarction (MI), and is expected to have more curative effects. Therefore, this study investigated the mechanism underlying cardioprotective role of 17β-estradiol NPs in rats with MI. After construction of rat MI model and preparation of 17β-estradiol NPs, the rats were administered with 17β-estradiol alone, 17β-estradiol NPs and Akt agonist or inhibitor. Distribution of 17β-estradiol NPs was observed by fluorescence microscope and release curve was detected. After treatment, echocardiography was conducted to measure the cardiac function indicators. With HE staining to observe myocardial tissue, RT-qPCR and Western blot determined levels of AKT and eNOS. The NPs were relatively uniform in size and round in shape; and cumulative release rate and concentration of 17β-estradiol in rats reached highest level on 30th day. Treatment with 17β-estradiol or 17β-estradiol NPs importantly increased survival rate of MI rats and decreased MI area while improving LVSP, LVDP, and HR. Moreover, the 17β-estradiol NPs had the smallest MI area. The myocardial tissue of rats in the 17β-estradiol NP group was closely arranged, and myocardial collagen was significantly reduced. The 17β-estradiol NPs increased the mRNA level of eNOS and Akt when eNOS expression was related to Akt expression. 17β-estradiol NPs can therefore increase the expression of eNOS by activating Akt signaling pathway, thereby relieving the myocardial injury in rats, hindering progression of MI.