Neurogenesis in rats after focal cerebral ischemia is enhanced by indomethacin

被引:224
|
作者
Hoehn, BD [1 ]
Palmer, TD [1 ]
Steinberg, GK [1 ]
机构
[1] Stanford Univ, Dept Neurosurg, Stanford, CA 94305 USA
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
收藏
页码:2718 / 2724
页数:7
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