期刊
NEUROREPORT
卷 12, 期 9, 页码 1919-1923出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00001756-200107030-00030
关键词
Akt; Alzheimer's disease; amyloid; estrogen; hippocampus; neuronal survival; neuroprotection
The cellular mechanisms underlying the neuroprotective effects of estrogen are only beginning to be elucidated. Here we examined the role of protein kinase B (Akt) activation in 17 beta -estradiol (E2) inhibition of beta -amyloid peptide (31-35) (A beta (31-35))induced neurotoxicity in cultured rat hippocampal neurons. A beta (31-35) (25-30 betaM) significantly decreased the total number of microtubule associated protein-2 positive cells (MAP2(+)). This decrease was significantly reversed by pre-treatment with 100 nM E2. Further, 100 nM E2 alone significantly increased the total number of protein kinase B and microtubule associated protein-2 positive cells compared with controls. Such E2-induced increases were inhibited by LY294002 (20 muM), a specific P13-K inhibitor, as well as by tamoxifen, an estrogen receptor antagonist/selective estrogen receptor modulator. These results indicate that the neuroprotective effects of E2 may be mediated at least in part via estrogen receptor-mediated protein kinase B activation. NeuroReport 12:1919-1923 (C) 2001 Lippinicott Williams & Wilkins.
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