Effects of 17β-estradiol replacement on the apoptotic effects caused by ovariectomy in the rat hippocampus

• Published in: Life sciences (1973) 2010-05, Vol.86 (21), p.832-838
• Main Authors: Sales, Sayuri, Ureshino, Rodrigo Portes, Pereira, Renato Tavares dos Santos, Luna, Milene Schmidt Amaral, Pires de Oliveira, Marcelo, Yamanouye, Norma, Godinho, Rosely Oliveira, Smaili, Soraya Soubhi, Porto, Catarina Segreti, Abdalla, Fernando Maurício Francis
• Format: Article
• Language: English
• Subjects: 17β-estradiol; Bax; Bcl-2; Hippocampus; Ovariectomy
• ISSN: 0024-3205; 1879-0631
• DOI: 10.1016/j.lfs.2010.04.002

The aim of the present study was to investigate the effects of different periods of ovariectomy and 17β-estradiol replacement on apoptotic cell death and expression of members of the Bcl-2 family in the rat hippocampus. Hippocampi were obtained from rats in proestrus, ovariectomized (15 days, 21 days and 36 days), ovariectomized for 15 days and then treated with 17β-estradiol for 7 or 21 days, and rats ovariectomized and immediately treated with 17β-estradiol for 21 days. The expression of Bcl-2 and Bax and the number of apoptotic cells were determined. Ovariectomy decreased Bcl-2 expression and increased Bax expression and the number of apoptotic cells. Replacement with 17β-estradiol (21 days) throughout the post-ovariectomy period reduced the number of apoptotic cells to the control levels, and prevented the effects of ovariectomy on Bax expression, but only partially restored the Bcl-2 expression. After 15 days of ovariectomy, the replacement with 17β-estradiol for 21 days, but not for 7 days, restored the Bcl-2 and Bax expression and the percentage of apoptotic cells to the levels found in the proestrus control. The present results show that a physiological concentration of 17β-estradiol may help maintain long-term neuronal viability by regulating the expression of members of the Bcl-2 family. Even after a period of hormonal deprivation, treatment with 17β-estradiol is able to restore the expression of Bax and Bcl-2 to control levels, but the duration of the treatment is a key factor to obtain the desired effect. These data provide new understanding into the mechanisms contributing to the neuroprotective action of estrogen.