局灶性脑缺血/再灌注后Fas、TNF-α在大鼠脑组织中的表达

目的 :通过观察局灶性脑缺血 /再灌注后大鼠脑组织中 Fas、肿瘤坏死因子 - α( TNF- α)的动态变化及细胞凋亡的情况 ,探讨脑缺血后 Fas、肿瘤坏死因子 - α与细胞凋亡的关系。方法 :采用大鼠大脑中动脉线栓动物模型 ,应用免疫组化及 TUNEL方法检测 Fas、TNF- α的动态变化和细胞凋亡情况并进行图像分析。结果 :局灶性脑缺血再灌注后 Fas过度表达 ,且在缺血再灌注后 6h达高峰 ,于 2 4 h开始下降 ;TNF- α的表达于再灌注 3h已有明显升高 ,2 4 h达到高峰 ,其后逐渐下降 ;细胞凋亡于再灌注 6h开始增加 ,2 4 h达到高峰 ,36h略有下降 ,且与 Fas及 TNF- α表达范围基本一致。结论 :Fas、TNF- α在局灶性脑缺血 /再灌注损伤中表达增加 ,介导细胞凋亡。它们在局灶性脑缺血再灌注损伤的病理过程中起到重要作用。

The expression of Fas and TNF-α in rat brain after focal cerebral ischemia/reperfusion

Objective: To observe the dynamic d iversification of Fas and TNF-α and cell apoptosis in rat brain after focal cerebral ischemia/ reperfusion an d to study the relationship among Fas , TNF-α and cell apoptosis after cerebra l ischemia. Methods: Focal cerebral ischemia (2 h)/reperfusion (24 h) model in rat s was induced by transient occlusion of middle cerebral artery (MCA) for 2 h and reperfusion for 36 h. Fas , TNF-α and cell apoptosis were detected at 3 h, 6 h, 12 h , 24 h and 36 h af te r the onset of reperfusion respectively. Immunochemistry and TUNEL were applied to detect dynamic diversification of Fas and TNF-α and cell apoptosis and make i mage analysis. Results: The expression of Fas increased excessively after cerebr al ischemia/ reperfusion, reached apex at 6 h after reperfusion and began to decrease at 24 h; The expression of TNF-α increased at 3 h after reperfusion, re ached apex at 24 h and then began to decrease; Cell apoptosis began to increase at 6 h after reperfusion, reached apex at 24 h and decreased in 36 h. The range of cell apoptosis was consistent with the expression of Fas and TNF-α. Conclu s ion: The expression of Fas and TNF-α increased in cerebral ischemia/ reperfusi on injury and interposed the cell apoptosis. They play an important role in the pathological process of focal cerebral ischemia/ reperfusion injury.