Nuclear transcription factor κB and phospholipase A2 in cerebral ischemia-reperfusion injury in the interaction.doc

 PAGE \* MERGEFORMAT 24 Nuclear transcription factor κB and phospholipase A2 in cerebral ischemia-reperfusion injury in the interaction Keywords: nuclear transcription factor κB phospholipase A2 cerebral ischemia-reperfusion Cerebral ischemia-reperfusion injury (Cerebral ischemia  reperfusion injury, CIRI) is excitatory (amino acid) poisoning, oxidative stress, intracellular calcium overload, inflammation and apoptosis (AP) and many other factors are involved in the pathological process of . CIRI mechanisms of the past, right in the former focused on three aspects, but in recent years with the development of molecular biology and found that CIRI and the inflammatory response and apoptosis also has a close relationship. Studies have shown that, CIRI is not only the occurrence of cell necrosis, but also an active and controlled by the genes, a series of enzymes involved in, the highly ordered process of dying, that is, the process of apoptosis, 50% of ischemic cell death is due to apoptosis. Nuclear transcription factor-κB is also called nuclear factor-k-gene binding (nuclear transcription factor κB, NF  κB), is a class of multi-gene promoter with parts of the κB site-specific binding occurred, and to promote the general transcription DNA-binding protein , is a multi-effect can be induced transcription factor, not only can regulate the expression of multiple genes and produce cytokines, but also regulate the expression of multiple inflammatory factors and cell apoptosis in ischemia-reperfusion injury play an important role. As inflammatory mediators, and active substances phospholipase A2 (phospholipids A2, PLA2), is a glycerol molecule can catalyze phospholipid hydrolysis of two acyl-enzyme is arachidonic acid (AA), prostaglandins and platelet activating factor (PAF) and other biologically active substances generated by rate-limiting enzyme, produced by lipid mediators in inflammation and tissue damage, the activation of the membrane chann