Abstract
Menopause is characterized by a decrease in estrogens production. These hormones show a cardio protective and antioxidant function. Menopause presents a high production of free radicals and a low antioxidant response, conducting to oxidative stress. It has been described that oxidative stress activates Nrf2, a transcription factor that in normal situations promotes antioxidant defense. It is suggested that Nrf2 actions promotes expression of cardioprotective antioxidant factors. Vascular protective effects of estrogen are due in part to the modulation of balance between nitric oxide and superoxide anion. In addition, estrogen induces the expression of thiol/disulfide oxide reductases, such as disulfide isomerase, thioredoxin, thioredoxin reductase and glutaredoxin in the endothelium and inhibits apoptosis mediated by hydrogen peroxide. However, the effect of estrogens absence upon the expression of Nrf2 and its probable participation in the development of cardiovascular diseases is still unknown. In this work, the effect of different types of hormone replacement therapy on the expression of Nrf2 in a model of ovariectomized rats is evaluated. The expression of Nrf2 was determined in left ventricle, renal cortex and aorta in ovariectomized rats with and without hormonal treatment using western blot and immunohistochemistry, also plasma levels of catalase, SOD, glutathione peroxidase and nitric oxide were measured in the same groups.There was a notable decrease in the expression of Nrf2 in the OVX group without treatment. Treatment groups showed an increase in native Nrf2 expression with respect to the ubiquitinized form. Plasmatic antioxidant enzymes (SOD, catalase and glutathione peroxidase), decreased in the OVX group, and were almost normal in treatment groups. Our findings indicate that hormone replacement treatment helps to re-establish the antioxidant enzymes production thru Nrf2 expression in cardiovascular system.
