脑缺血或缺血再灌注后,常继发脑细胞的大量死亡,炎性细胞浸润、炎性因子的释放,炎性反应在其中起到了关键性作用。核因子κB在炎性反应中处于中心环节,它过度激活加重缺血损伤。近年来研究发现,脑缺血预处理可诱导脑缺血耐受能力,其作用机制可能与脑缺血预处理干预了脑缺血后核因子κB及其相关炎性反应、上调保护性因子生成、参与细胞凋亡途径通路的调节、降低脑损伤作用有关。 Cerebral ischemia or ischemia-reperfusion, often secondary to a large number of brain cell death, inflammatory cell infiltration, the release of inflammatory cytokines, inflammatory reactions in which play a key role. Nuclear factor kappa B is at the center of the inflammatory response and is over-activated to aggravate ischemic injury. In recent years, studies have found that cerebral ischemic preconditioning can induce cerebral ischemic tolerance, the mechanism may be related to cerebral ischemia preconditioning intervention of nuclear factor kappa B and its related inflammatory response, up-regulate the generation of protective factors , Participate in the regulation of pathways of apoptosis and reduce the effect of brain injury.