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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

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

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Author(s):
Sales, Sayuri [1] ; Ureshino, Rodrigo Portes [2] ; dos Santos Pereira, Renato Tavares [1] ; Amaral Luna, Milene Schmidt [1] ; de Oliveira, Marcelo Pires [2] ; Yamanouye, Norma [1] ; Godinho, Rosely Oliveira [2] ; Smaili, Soraya Soubhi [2] ; Porto, Catarina Segreti [2] ; Francis Abdalla, Fernando Mauricio [1]
Total Authors: 10
Affiliation:
[1] Inst Butantan, Pharmacol Lab, BR-05503900 Sao Paulo - Brazil
[2] Univ Fed Sao Paulo, Dept Pharmacol, Escola Paulista Med, Sao Paulo - Brazil
Total Affiliations: 2
Document type: Journal article
Source: Life Sciences; v. 86, n. 21-22, p. 832-838, MAY 22 2010.
Web of Science Citations: 16
Abstract

Aims: The aim of the present study was to investigate the effects of different periods of ovariectomy and 17 beta-estradiol replacement on apoptotic cell death and expression of members of the Bcl-2 family in the rat hippocampus. Main methods: Hippocampi were obtained from rats in proestrus, ovariectomized (15 days, 21 days and 36 days), ovariectomized for 15 days and then treated with 17 beta-estradiol for 7 or 21 days, and rats ovariectomized and immediately treated with 17 beta-estradiol for 21 days. The expression of Bcl-2 and Bax and the number of apoptotic cells were determined. Key findings: Ovariectomy decreased Bcl-2 expression and increased Bax expression and the number of apoptotic cells. Replacement with 17 beta-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 17 beta-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. Significance: The present results show that a physiological concentration of 17 beta-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 17 beta-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. (C) 2010 Elsevier Inc. All rights reserved. (AU)

FAPESP's process: 03/10132-0 - Estrogen and colinergic muscarinic neurotransmission: expression of receptors, intracellular signaling and its interactions in the central nervous system and in the male reproductive tract
Grantee:Catarina Segreti Porto
Support Opportunities: PRONEX Research - Thematic Grants