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Role of cyclooxygenase-2 inhibition in regulating the inflammatory response to intracerebral hemorrhage. Inflammation is a key component of intracerebral hemorrhage (ICH) pathophysiology. However, the effect of cyclooxygenase-2 (COX-2) inhibition on inflammation in this disease is unclear. In a model of ICH, the dose-dependent effect of COX-2 inhibition on cerebral edema, leukocyte recruitment, and glial activation was assessed. COX-2 inhibition was associated with dose-dependent reductions in brain water content, leukocyte infiltration, and glial activation. These effects were specific to ICH, as COX-2 inhibition had no effect on brain edema in a model of collagenase-induced cerebral microbleeds or on leukocyte recruitment in an experimental autoimmune encephalomyelitis model. The involvement of COX-2 in the inflammatory response to ICH is both tissue and dose dependent. Inhibition of COX-2 reduces edema and leukocyte recruitment but has no effect on glial activation. These findings demonstrate the specific influence of COX-2 on the inflammatory response in ICH.

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