Reduced susceptibility to ischemic brain injury and N -methyl- d -aspartate-mediated neurotoxicity in cyclooxygenase-2-deficient mice

• DOI: 10.1073/pnas.98.3.1294
• Publication Date: 2002-07-26T14:45:09Z
• Authors: Costantino Iadecola; Kiyoshi Niwa; Shigeru Nogawa; Xueren Zhao; Masao Nagayama; Eiichi Araki; Scott Morham; M. Elizabeth Ross
• Keywords: Neurotoxicity; Stroke; Brain ischemia; Prostanoid

Cyclooxygenase-2 (COX-2), a prostanoid-synthesizing enzyme that contributes to the toxicity associated with inflammation, has recently emerged as promising therapeutic target for several illnesses, ranging from osteoarthritis Alzheimer's disease. Although COX-2 also been linked ischemic stroke, its role in mechanisms of brain injury remains controversial. We demonstrate COX-2-deficient mice have significant reduction produced by occlusion middle cerebral artery. The protection can be attributed attenuation glutamate neurotoxicity, critical factor initiation injury, and abrogation deleterious effects postischemic process contributing secondary progression damage. Thus, is involved pathogenic events occurring both early late stages ischemia may valuable treatment human stroke.