| In cerebral ischemic stroke, there are ischemic injury and reperfusion injury. Recent studys have revealed that inflammatory mechanisms play an important role in the secondary injury after acute cerebral ischemia, which was characterized by a progressive increase in neutrophils adhesion and infiltration. Inflammatory cytokines as well as adhesion molecules which are produced at the early stage of ischemia promote both the recruitment of inflammatory cells, their adherence to brain endothelial cells and the resultant activation of inflammatory processes. In recent years, activated microglia following cerebral ischemia/reperfusion (CIRP) has caught a lot of attention. Experiments showed that microglia were the first cell responding to the ischemic injury. Most of cytokines from activated microglia, such as TNF-αand IL-1β, have neurotoxic action and inflammation-causing effects. Matrix metalloproteinase-3 (MMP-3) and osteopontin (OPN) that are up-regulated in the early stage of ischemic brain damage are closely related to microglia and involved in inflammatory reaction. Recent reserachs discovered that aspirin (ASA) had the direct neuroprotective effects besides its antiplatelet effect during the treatment of ischemic stroke. ASA is traditionally thought of as an inflammatory inhibitor by inhibiting cycloxygenase (COX), especially COX-2. Experimentally, aspirin can prevent glutamate-induced neurotoxicity via blockade of NF-κB induction, which lends support to aspirin having more actions than COX inhibition. But so far as we know, there is no report on ASA's effects on activation of microglia as well as express of MMP-3 and...
|
PDF Full Text Request