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目的:探讨脑组织肿瘤坏死因子ɑ(TNFɑ)过度表达对小胶质细胞、星形胶质细胞激活及脑缺血梗死灶体积的影响。方法:用TNFɑ、胶质纤维酸性蛋白(GFAP)、髓磷脂、整合素ɑM(OX42)免疫组化染色观察SD大鼠与转小鼠TNFɑ基因大鼠未缺血脑组织的TNFɑ表达及3种神经胶质细胞穴星形胶质细胞、小胶质细胞与少突神经胶质细胞雪的激活状态。采用线栓法制作大鼠大脑中动脉闭塞模型,SD大鼠与转小鼠TNFɑ基因大鼠缺血1h再灌注72h后,先行神经功能缺损程度评分,再断头取脑四氯氮唑(TTC)染色计算脑梗死体积。结果:转小鼠TNFɑ基因大鼠与SD大鼠相比,未缺血脑组织见TNFɑ表达,且星形胶质细胞、小胶质细胞与少突神经胶质细胞呈肥大和增生性变化;缺血1h再灌注72h后神经功能缺损程度评分显著增高,脑梗死灶体积显著增大。结论:未缺血时脑组织TNFɑ的表达可明显激活3种神经胶质细胞,TNFɑ的过度表达可使脑缺血时神经功能明显恶化及脑梗死体积明显增加,提示TNFɑ的过度表达可明显加剧缺血性脑损伤。
Objective: To investigate the effects of overexpression of tumor necrosis factor (TNF) in brain on the activation of microglia and astrocyte and the volume of cerebral infarction. Methods: Immunohistochemical staining of TNFα, glial fibrillary acidic protein (GFAP), myelin and integrin ɑM (OX42) was used to observe the expression of TNFɑ in non-ischemic brain tissue of SD rats and mice with TNFɑ Activation of glial cells in astrocytes, microglia and oligodendrocytes. The rat model of middle cerebral artery occlusion (MCAO) was established by thread occlusion. Rats in SD rats and mice with TNF ¢ ò gene were reperfused for 1 hour and then reperfusion for 72 hours. ) Staining to calculate the volume of cerebral infarction. Results: Compared with SD rats, the expression of TNFɑ in non-ischemic brain tissue of rats with TNFɑ transgenic mice showed hypertrophic and proliferative changes astrocytes, microglia and oligodendrocytes; After 1h of ischemia and 72h of reperfusion, the score of neurological deficit was significantly increased, and the volume of cerebral infarction was significantly increased. CONCLUSION: The expression of TNF 脑 in the brain tissue without ischemia can activate three kinds of glial cells. Overexpression of TNF 可 can significantly worsen the neurological function and increase the volume of cerebral infarction. It suggests that TNF ɑ overexpression may be significantly increased Ischemic brain injury.