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

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

Author Sales, Sayuri Google Scholar
Ureshino, Rodrigo Portes Autor UNIFESP Google Scholar
Santos Pereira, Renato Tavares dos Google Scholar
Amaral Luna, Milene Schmidt Google Scholar
Oliveira, Marcelo Pires de Autor UNIFESP Google Scholar
Yamanouye, Norma Google Scholar
Godinho, Rosely Oliveira Autor UNIFESP Google Scholar
Smaili, Soraya Soubhi Autor UNIFESP Google Scholar
Porto, Catarina Segreti Autor UNIFESP Google Scholar
Francis Abdalla, Fernando Mauricio Google Scholar
Institution Inst Butantan
Universidade Federal de São Paulo (UNIFESP)
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.
Keywords Bcl-2
Bax
Hippocampus
17 beta-estradiol
Ovariectomy
Language English
Sponsor Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
Grant number FAPESP: 03/10132-0
Date 2010-05-22
Published in Life Sciences. Oxford: Pergamon-Elsevier B.V., v. 86, n. 21-22, p. 832-838, 2010.
ISSN 0024-3205 (Sherpa/Romeo, impact factor)
Publisher Elsevier B.V.
Extent 832-838
Origin http://dx.doi.org/10.1016/j.lfs.2010.04.002
Access rights Closed access
Type Article
Web of Science ID WOS:000277809500009
URI http://repositorio.unifesp.br/handle/11600/32549

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