【摘要】 再灌注损伤是由多种原因引起的复杂的病理生理过程,而级联的炎症反应是导致脑细胞损伤的重要病理环节。脑缺血再灌注后,浸润的炎性细胞产生的大量炎性介质,在再灌注损伤中占有重要地位。肿瘤坏死因子α(TNF-α)是一种具有广泛生物学功能的细胞因子,参与机体免疫应答和炎症反应TNF-α是细胞间粘附分子-1(ICAM-1)表达的强诱导剂,抑制细胞粘附分子(ICAM-1)表达可显著减低再灌注时白细胞粘附活化,减少损伤脑面积起保护作用。粒细胞集落刺激因子(G-CSF)能通过STAT途径减少缺血区肿瘤坏死因子-α等的释放,引起人们对其在脑缺血-再灌注损伤中的作用的极大关注。更多还原

【Abstract】 Reperfusion injury is a complex pathophysiological process with many causes.But the cascade of inflammatory reactions are important pathological aspects causing brain cell damage.After cerebral ischemia and reperfusion,inflammatory cells produce a large number of inflammatory mediators,which play an important role in reperfusion injury.Tumor necrosis factor(TNF-a) is a cytokine which has a wide range of biological functions,involving in the immune response and inflammatory responses.Tumor necrosis factor-α(TNF-a) is the strong inducer of intercellular adhesion molecule-1(ICAM-1) expressed,Inhibition of cell adhesion molecules(ICAM-1) expression can significantly reduce leukocyte adhesion activation when reperfusing,reducing the area of damaged brain play a protective role.Granulocyte colony stimulating factor(G-CSF)reduces the release of TNF-α etc.in the ischemic area through the STAT pathway,thereby G-CSF has an anti-inflammatory effects on reducing the activation of neutrophils,thus causing great concern about its role in the mechanism of cerebral ischemia-reperfusion injury.更多还原