Neurogenesis in rats after focal cerebral ischemia is enhanced by indomethacin

被引：225

作者：

Hoehn, BD ^{[1
]}

Palmer, TD ^{[1
]}

Steinberg, GK ^{[1
]}

机构：

[1] Stanford Univ, Dept Neurosurg, Stanford, CA 94305 USA

来源：

STROKE | 2005年 / 36卷 / 12期

关键词：

brain infarction; brain ischemia; indomethacin; inflammation; ischemia; neurogenesis; stroke;

D O I：

10.1161/01.STR.0000190020.30282.cc

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

Background and Purpose - Newborn cells may participate in repair following ischemic brain injury, but their survival and function may be influenced by inflammation. Methods - We investigated the effects of indomethacin, a nonsteroidal antiinflammatory drug, on the fate of newborn cells following transient focal ischemia. Results - Bromodeoxyuridine ( BrdU)- labeled cells, including migrating neuroblasts, were observed in the neighboring striatum and overlying cortex 1 day poststroke. The density of BrdU+ cells labeled with doublecortin, nestin, glial fibrillary acidic protein, or NG2 was increased at 14 and 28 days. Indomethacin increased BrdU+ cells of all lineages and reduced microglial/monocyte activation. Conclusion - Indomethacin enhanced the accumulation of newborn cells following stroke.

引用

页码：2718 / 2724

页数：7

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