Selective inhibition of cyclooxygenase-2 attenuates expression of inflammation-related genes in CNS injury.

Abstract

Injury to the brain, whether arising from trauma, stroke, or infection, elicits a tissue response characterized by glial cell activation and production of inflammation-related gene products. A similar response occurs in Alzheimer’s disease, where deposits of amyloid-beta are associated with activated glia and a wide variety of inflammatory products have been detected (Neuroinflammation Working Group, 2000). The widespread use of glucocorticoids in spinal cord injury and epidemiological evidence that nonsteroidal anti-inflammatory drugs may be beneficial in Alzheimer’s disease indicate that therapies targeting inflammatory processes may be useful in treatment of central nervous system (CNS) injury and disease. Cyclooxygenase-2 (COX-2) plays a major role in peripheral inflammatory processes (Dubois et al., 1998). Tissue culture studies show that astrocytes and microglia have the capacity to express COX-2 in response to proinflammatory cytokines (O’Banion et al., 1996; O’Banion, 1999). However, little is known about the contribution of COX-2 to inflammatory processes in the CNS.KeywordsTraumatic Brain InjuryCentral Nervous System InjuryGlial ActivationTissue Culture StudyGlial Cell ActivationThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.