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Results from several studies indicate that cyclooxygenase-2 (COX-2) isinvolved in ischemic brain injury. The purpose of this study was to evaluatethe neuroprotective effects of the selective COX-2 inhibitor nimesulide oncerebral infarction and neurological deficits in a standardized model oftransient focal cerebral ischemia in rats. Three doses of nimesulide (3, 6 and12 mg/kg; i.p.) or vehicle were administered immediately after stroke andadditional doses were given at 6, 12, 24, 36 and 48 h after ischemia. In otherset of experiments, the effect of nimesulide was studied in a situation inwhich its first administration was delayed for 3-24 h after ischemia. Total,cortical and subcortical infarct volumes and functional outcome (assessed byneurological deficit score and rotarod performance) were determined 3 daysafter ischemia. The effect of nimesulide on prostaglandin E(2) (PGE(2)) levelsin the injured brain was also investigated. Nimesulide dose-dependently reducedinfarct volume and improved functional recovery when compared to vehicle. Ofinterest is the finding that neuroprotection conferred by nimesulide (reductionof infarct size and neurological deficits and improvement of rotarodperformance) was also observed when treatment was delayed until 24 h afterischemia. Further, administration of nimesulide in a delayed treatment paradigmcompletely abolished PGE(2) accumulation in the postischemic brain, suggestingthat COX-2 inhibition is a promising therapeutic strategy for cerebral ischemiato target the late-occurring inflammatory events which amplify initial damage.

Wide therapeutic time window for nimesulide neuroprotection in a model of transient focal cerebral ischemia in the rat