Neurogenesis in rats after focal cerebral ischemia is enhanced by indomethacin

Stroke. 2005 Dec;36(12):2718-24. doi: 10.1161/01.STR.0000190020.30282.cc. Epub 2005 Nov 10.

Abstract

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.

Conclusions: Indomethacin enhanced the accumulation of newborn cells following stroke.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology*
  • Biomarkers / metabolism
  • Cell Count
  • Cell Division / drug effects
  • Cell Lineage / drug effects
  • Cerebral Cortex / pathology
  • Corpus Striatum / pathology
  • Doublecortin Protein
  • Immunologic Factors / pharmacology
  • Indomethacin / pharmacology*
  • Inflammation / immunology
  • Ischemic Attack, Transient / pathology*
  • Ischemic Attack, Transient / physiopathology
  • Lymphocyte Activation / drug effects
  • Male
  • Microglia / drug effects
  • Microglia / pathology
  • Monocytes
  • Neurons / drug effects*
  • Neurons / metabolism
  • Rats
  • Rats, Sprague-Dawley

Substances

  • Anti-Inflammatory Agents, Non-Steroidal
  • Biomarkers
  • Dcx protein, rat
  • Doublecortin Protein
  • Immunologic Factors
  • Indomethacin