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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。
Objective: To investigate the role of inflammatory response in cerebral arterial micro-emboli-induced neuronal damage in the brain. Methods: Forty eight Sprague-Dawley rats were randomly divided into three groups: micro-emboli 3d, micro-emboli 7d, sham-operated 3d, and sham-operated 7d (n = 12). Microembolization group 25 ~ 50μm whole blood clot microinjection into the left internal carotid artery of SD rats to establish a model of cerebral injury induced by micro-emboli under the threshold of cerebral infarction. The rats were sacrificed on day 3 and day 7 after injury. Immunohistochemical staining of CD11b and GFAP was used to quantify the proliferation and activation of microglia and astrocytes. The expression of TNF-α was detected by ELISA. The expression of NF-κB expression. Results: Cerebral injury induced by micro-emboli in cerebral infarction threshold rat model, microglial cells and astrocytes proliferated obviously (P <0.001), and more obvious in 7d group than in 3d group (P <0.001). The expression of TNF-α and NF-κB were significantly increased (P <0.001). The levels of TNF-α and NF-κB in 3d group were significantly higher than those in 7d group (P <0.001). CONCLUSION: The proliferation and activation of microglia and astrocytes and the involvement of TNF-α and NF-κB play an important role in the pathogenesis of neuronal apoptosis induced by cerebral arterial microembolism.