TNF-α与G-CSF在脑缺血-再灌注损伤中的研究

Study on TNF-α and G-CSF in the Cerebral Ischemia-Reperfusion Injury

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。

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 e erebral ischemia and reperfusion, in flammatory cells produce a large number of inflammatory mediators, which play an important role in reperfusion injury. Tumor necrosis factor（TNF-α） is a cytokine which has a wide range of biological fimctions, involving in the immune response and inflammatory responses. Tumor necrosis factor-α （TNF-α） is the strong inducer of intercellular adhesion molecule -1 （ICAM-1） expressed, Inhibition of cell adhesion molecules （ICAM-I） 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 eoneem about its role in the mechanism of cerebral ischemia - reperfusion injury.