脑缺血预处理对核因子κB相关炎性反应作用研究  

The Effect of Cerebral Ischemic Preconditioning on NF-κB related Inflammatory Reaction

作　　者：梁炳松[1] 毕桂南[1] 

机构地区：[1]广西医科大学第一附属医院神经内科,南宁530021

出　　处：《医学综述》2007年第23期1761-1763,共3页Medical Recapitulate

基　　金：广西科学基金(桂科自0542091)

摘　　要：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 and ischemie reperfusion will result in mass mortality of brain cell, inflammatory cell infiltration and inflammatory factors） releasing, in which the infiammatory reaction plays the key role. Nuclear factor-kappa B plays the central role in inflammatory, reaction, of which the over activation will aggravate the ischemic injury. The recent researches show that cerebral isehemie preconditioning can indue increased tolerance to cerebral isehemic, of which the mechanism maybe associate with many factors including inhibiting nuclear factor-kappa B and its inflammatory reaction, upregulating the genesis of protective factors, takiing part in the regulation of cell apoptosis pathway and decreasing brain injury.

关 键 词：脑缺血 预处理 炎性反应 核因子ΚB 

分 类 号：R743.9[医药卫生—神经病学与精神病学]