@misc{cogprints5393,
          volume = {100},
          number = {4},
           month = {February},
          author = {Eduardo Candelario-Jalil and Armando Gonzalez-Falcon and Michel Garcia-Cabrera and Olga Sonia Leon and Bernd Fiebich},
          editor = {Prof. Sean Murphy and Prof. Anthony Turner},
           title = {Post-ischaemic treatment with the cyclooxygenase-2 inhibitor nimesulide reduces blood-brain barrier disruption and leukocyte infiltration following transient focal cerebral ischaemia in rats},
       publisher = {Blackwell Publishing},
            year = {2007},
         journal = {Journal of Neurochemistry},
           pages = {1108--1120},
        keywords = {Cyclooxygenase; prostaglandin E2; stroke; blood-brain barrier; leukocyte infiltration; cerebral ischemia; vasogenic edema; cerebral infarct; neuroprotection; prostanoids; COX-2; COX-1; neurodegeneration},
             url = {http://cogprints.org/5393/},
        abstract = {Several studies suggest that cyclooxygenase (COX)-2 plays a pivotal role in the progression of ischemic brain damage. In the present study, we investigated the effects of selective inhibition of COX-2 with nimesulide (12 mg/kg) and selective inhibition of COX-1 with valeryl salicylate (VAS, 12-120 mg/kg) on prostaglandin E2 (PGE2) levels, myeloperoxidase (MPO) activity, Evans Blue (EB) extravasation and infarct volume in a standardized model of transient focal cerebral ischemia in the rat. Postischemic treatment with nimesulide markedly reduced the increase in PGE2 levels in the ischemic cerebral cortex 24 h after stroke and diminished infarct size by 48 \% with respect to vehicle-treated animals after 3 days of reperfusion. Furthermore, nimesulide significantly attenuated the blood-brain barrier (BBB) damage and leukocyte infiltration (as measured by EB leakage and MPO activity, respectively) seen at 48 h after the initial ischemic episode. These studies provide the first experimental evidence that COX-2 inhibition with nimesulide is able to limit BBB disruption and leukocyte infiltration following transient focal cerebral ischemia. Neuroprotection afforded by nimesulide is observed even when the treatment is delayed until 6 h after the onset of ischemia, confirming a wide therapeutic window of COX-2 inhibitors in experimental stroke. On the other hand, selective inhibition of COX-1 with VAS had no significant effect on the evaluated parameters. These data suggest that COX-2 activity, but not COX-1 activity, contributes to the progression of focal ischemic brain injury, and that the beneficial effects observed with non-selective COX inhibitors are probably associated to COX-2 rather than to COX-1 inhibition. }
}

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