Estradiol protects against oxygen and glucose deprivation in rat hippocampal organotypic cultures and activates Akt and inactivates GSK-3beta.
Neurochem Res
; 30(2): 191-9, 2005 Feb.
Article
em En
| MEDLINE
| ID: mdl-15895822
Here we investigated the neuroprotective effect of 17beta-estradiol in an in vitro model of ischemia. We used organotypic hippocampal slice cultures, acute or chronically treated with 17beta-estradiol (10 nM), and exposed to oxygen and glucose deprivation (OGD). Cellular death was quantified by measuring uptake of propidium iodide (PI), a marker of dead cells. In OGD exposed cultures, treated only with vehicle, about 70% of the CA1 area of hippocampus was labeled with PI, indicating a great percentage of cellular death. When cultures were treated with 17beta-estradiol (acute or chronically), this cellular death was reduced to 15%. This effect was prevented by LY294002 but was not by PD98059. Immunoblotting revealed that both, chronic and acute, treatments with 17beta-estradiol induced the phosphorylation/activation of Akt and the phosphorylation/inactivation of GSK-3beta. Our results show a clear neuroprotective effect of 17beta-estradiol and suggest that this effect could involve PI3-K pathway.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Proteínas Proto-Oncogênicas
/
Proteínas Serina-Treonina Quinases
/
Fármacos Neuroprotetores
/
Quinase 3 da Glicogênio Sintase
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Estradiol
/
Glucose
/
Hipocampo
/
Hipóxia
Limite:
Animals
Idioma:
En
Revista:
Neurochem Res
Ano de publicação:
2005
Tipo de documento:
Article
País de afiliação:
Brasil
País de publicação:
Estados Unidos