The Biochemical and histopathological effects of estrogen replacement therapy on the heart of ovariectomized female rats subjected to myocardial infarction

Abstract

Objective The aim of this study was to evaluate the biochemical and histopathological effects of estrogen replacement therapy on the heart of ovariectomized female rats subjected to myocardial infarction. Methods Sixty young (30 days old) and adult (60 days old) female rats weighing 150–200 g were taken for the study and divided into three groups: group I, sham-operated rats; group II, ovariectomized (OVX) and isoproterenol (ISO) induced myocardial infarction (MI) rats; and group III, OVX and ISO induced MI rats treated with 17β-estradiol (E2), with each group comprising 20 rats (n=20). Four weeks after ovariectomy, isoproterenol was injected subcutaneously at a dose of 150 mg/kg/day for 2 successive days into the rats to induce MI. The rats in group III were injected intraperitoneally with 10 µg/kg/day E2 for 10 weeks. Electrocardiograms (ECG) was conducted 12 h after the second dose of isoproterenol. Biochemical estimation of plasma creatine kinase (CPK) and lactate dehydrogenase (LDH) levels was carried out. The hearts of the rats were collected for clinical biochemical analyses, which include measuring the levels of malondialdehyde (MDA) in tissue, enzymatic antioxidants such as superoxide dismutase (SOD) and catalase (CAT), and nonenzymatic antioxidants such as reduced glutathione (GSH), and were studied histopathologically by light and electron microscopy, as well as by immunohistochemical analysis. Results Plasma CPK, LDH and MDA levels were highly significantly increased in the ovariectomy and ISO induced MI group II compared with the control group I, but significantly decreased in ovariectomy and ISO induced MI treated E2 group III. In contrast, levels of SOD, CAT and GSH were highly significantly decreased in the ovariectomy and ISO induced MI group II compared with the control group I, but significantly increased in the ovariectomy and isoproterenol induced MI treated E2 group III. Histopathological analysis of the hearts of ovariectomized and ISO induced MI rats showed pathological changes. However, treatment with E2 attenuated the histopathological changes and corrected the biochemical parameters mentioned above. Conclusion 17β-estradiol E2 has a cardioprotective effect; it has been shown to inhibit structural and functional aspects of MI and attenuate the oxidative stress involved in isoproterenol-induced MI.