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(Stroke. 2005;36:2718.)
© 2005 American Heart Association, Inc.

Original Contributions

Neurogenesis in Rats After Focal Cerebral Ischemia is Enhanced by Indomethacin

From the Department of Neurosurgery, Stanford University, Stanford, Calif.

Correspondence to Gary K. Steinberg, MD, PhD, Department of Neurosurgery, 300 Pasteur Drive, MC: 5327, Stanford, CA 94305-5327. E-mail gsteinberg{at}stanford.edu

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.

Key Words: brain infarction • brain ischemia • indomethacin • inflammation • ischemia • neurogenesis • stroke

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