Neurones treated with cyclo-oxygenase-1 inhibitors are resistant to amyloid-β1-42

被引:23
作者
Bate, C
Veerhuis, R
Eikelenboom, P
Williams, A
机构
[1] Univ Glasgow, Sch Vet, Dept Vet Pathol, Inst Comparat Med, Glasgow G61 1QH, Lanark, Scotland
[2] Vrije Univ Amsterdam, Med Ctr, Grad Sch Neurosci Amsterdam, Dept Pathol, Amsterdam, Netherlands
[3] Vrije Univ Amsterdam, Med Ctr, Grad Sch Neurosci Amsterdam, Dept Psychiat, Amsterdam, Netherlands
关键词
amyloid-beta; cyclo-oxygenase-1; neurotoxicity; prostaglandins;
D O I
10.1097/00001756-200311140-00018
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Epidemiological studies have shown that the risk of developing Alzheimer's disease is reduced by the chronic use of classical non-steroidal anti-inflammatory drugs (NSAIDs), drugs that inhibit the cyclo-oxygenase (COX) enzymes that convert arachidonic acid to prostaglandins. In the present study, human SH-SY5Y neuroblastoma cells or murine primary cortical neurones treated with NSAIDs were protected against the otherwise toxic effects of amyloid-beta(1-42). COX-1 selective inhibitors provided greater protection than did COX-2 selective inhibitors or lipoxygenase inhibitors, suggesting that activation of COX-1 is required for amyloid-beta(1-42)-induced neurotoxicity. Although the production of neuronal prostaglandin E-2 in response to amyloid-beta(1-42) was reduced by the presence of COX-1 inhibitors, no neurotoxic effects of prostaglandin E-2, or any other prostaglandin, were observed.
引用
收藏
页码:2099 / 2103
页数:5
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