炎症反应在脑动脉微栓子导致的大脑神经元损伤机制中的作用  

The Role of Inflammation in the Neuronal Injury Induced by Cerebral Arterial Microemboli

作　　者：吴亦影[1] 卞雷斯[1] 宁敏[1] 倪秀石[1] 

机构地区：[1]上海交通大学附属第一人民医院老年科,200080

出　　处：《中国临床神经科学》2011年第1期16-22,共7页Chinese Journal of Clinical Neurosciences

摘　　要：目的:探讨炎症反应在脑动脉微栓子导致的大脑神经元损伤机制中的作用。方法:48只SD大鼠随机分为微栓子3d组、微栓子7d组、假手术3d组和假手术7d组(均n=12)。微栓子组将25～50μm全血凝块微栓子注入SD大鼠左侧颈内动脉,建立脑梗死阈值下微栓子导致的脑损伤模型。损伤后3d和7d分批处死大鼠,CD11b和GFAP蛋白免疫组化染色定量分析小胶质细胞和星形胶质细胞的增生活化,ELISA检测TNF-α的表达,Western blot检测NF-κB的表达。结果:脑梗死阈值下微栓子导致的脑损伤大鼠模型,小胶质细胞和星型胶质细胞明显增生活化(P<0.001),7d组比3d组更明显(P<0.001)。TNF-α和NF-κB的表达明显增加(P<0.001),3d组比7d组更明显(P<0.001)。结论:小胶质细胞和星形胶质细胞的增生活化以及TNF-α和NF-κB的参与在脑动脉微栓子导致的神经元凋亡的发病机制中起重要作用。Aim：To explore the role of inflammation in the neuronal injury induced by cerebral arterial microemboli. Methods：The brain injury rat models without infarction were established by being injected the microemboli in size of 25-50 mm from whole blood clots via left internal carotid arteries. The rats were executed on the 3rd day and 7th day separately. Activation of microglia and astrocytes were quantitated with immunohistochemistry staining of GFAP and CD11b. TNF-a expression was assessed with enzyme-linked immunosorbant assay （ELISA）. NF-κB was determined with Western blot. Results：Activation of microglia and astrocytes shown a significant increase in the microembous group compared with the sham group（P0.001）. TNF-a and NF-κB expression were more obvious in the microembous group than the sham group（P0.001）. Conclusion：Activation of microglia and astrocytes,as well as the higher expression of TNF-a and NF-κB play important roles in the mechanism of neuronal apoptosis induced by cerebral arterial microemboli.

关 键 词：微栓子 炎症反应 神经元凋亡 大鼠模型 

分 类 号：R743[医药卫生—神经病学与精神病学]