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Several studies suggest that cyclooxygenase (COX)-2 plays a pivotal role inthe progression of ischaemic brain damage. In the present study, weinvestigated the effects of selective inhibition of COX-2 with nimesulide (12mg/kg) and selective inhibition of COX-1 with valeryl salicylate (VAS, 12-120mg/kg) on prostaglandin E2 (PGE2) levels, myeloperoxidase (MPO) activity, Evansblue (EB) extravasation and infarct volume in a standardized model of transientfocal cerebral ischaemia in the rat. Post-ischaemic treatment with nimesulidemarkedly reduced the increase in PGE2 levels in the ischaemic cerebral cortex24 h after stroke and diminished infarct size by 48% with respect tovehicle-treated animals after 3 days of reperfusion. Furthermore, nimesulidesignificantly attenuated the blood-brain barrier (BBB) damage and leukocyteinfiltration (as measured by EB leakage and MPO activity, respectively) seen at48 h after the initial ischaemic episode. These studies provide the firstexperimental evidence that COX-2 inhibition with nimesulide is able to limitBBB disruption and leukocyte infiltration following transient focal cerebralischaemia. Neuroprotection afforded by nimesulide is observed even when thetreatment is delayed until 6 h after the onset of ischaemia, confirming a widetherapeutic window of COX-2 inhibitors in experimental stroke. On the contrary,selective inhibition of COX-1 with VAS had no significant effect on theevaluated parameters. These data suggest that COX-2 activity, but not COX-1activity, contributes to the progression of focal ischaemic brain injury, andthat the beneficial effects observed with non-selective COX inhibitors areprobably associated to COX-2 rather than to COX-1 inhibition.

Post-ischaemic treatment with the cyclooxygenase-2 inhibitor nimesulide  reduces blood-brain barrier disruption and leukocyte infiltration following  transient focal cerebral ischaemia in rats