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 17b-estradiol (E2), with each
group comprising 20 rats (n=20). Four weeks after ovariectomy, isoproterenol was
injected subcutaneously at a dose of 150mg/kg/day for 2 successive days into the rats
to induce MI. The rats in group III were injected intraperitoneally with 10 mg/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
17b-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.