Estradiol protects against oxygen and glucose deprivation in rat hippocampal organotypic cultures and activates Akt and inactivates GSK-3β

被引：47

作者：

Cimarosti, H ^{[1
]}

Zamin, LL ^{[1
]}

Frozza, R ^{[1
]}

Nassif, M ^{[1
]}

Horn, AP ^{[1
]}

Tavares, A ^{[1
]}

Netto, CA ^{[1
]}

Salbego, C ^{[1
]}

机构：

[1] Univ Fed Rio Grande do Sul, Inst Ciencias Basicas Saude, Dept Bioquim, BR-90035003 Porto Alegre, RS, Brazil

来源：

NEUROCHEMICAL RESEARCH | 2005年 / 30卷 / 02期

关键词：

cerebral ischemia; 17; beta-estradiol; organotypic hippocampal culture; Akt; GSK-3; beta; neuroprotection;

D O I：

10.1007/s11064-004-2441-y

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Here we investigated the neuroprotective effect of 17 beta-estradiol in an in vitro model of ischemia. We used organotypic hippocampal slice cultures, acute or chronically treated with 17 beta-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 17 beta-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 17 beta-estradiol induced the phosphorylation/activation of Akt and the phosphorylation/inactivation of GSK-3 beta. Our results show a clear neuroprotective effect of 17 beta-estradiol and suggest that this effect could involve PI3-K pathway.

引用

页码：191 / 199

页数：9

共 49 条

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