Role of Inducible Nitric Oxide Synthase and Cyclooxygenase-2 in the Mechanisms of Ischemic Brain Injury

摘要: There is a growing body of evidence indicating that cerebral ischemic damage associated with local inflammatory reaction, which contributes to the development brain injury. We review inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) are involved in mechanisms by ischemia-induced inflammation tissue damage. In rodents, as humans, iNOS expressed cells infiltrating blood vessels. Administration inhibitors 24h after ischemia reduces size infarct produced occlusion rat middle artery (MCA). Furthermore, “knockout” mice lacking gene have smaller infarcts than wild-type mice. COX-2 postischemic time course similar iNOS; it present neurons, cells, selective inhibitor NS-398 size. NO activates COX-2, thereby increasing production toxic prostanoids free radicals. The suggests synthesized iNOS, part through reaction products expansion occurs during late period. Thus, interaction between plays an important role stages Delayed administration may be useful therapeutic strategy target selectively progression