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.
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.