摘要
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 explore the effects of overexpression of murine tumor necrosis factor-ɑ(TNFɑ) gene of Sprague-Dawley(SD) transgenic rats on glia and infarct volume in focal cerebral ischemia. Methods: Protein expression of TNFɑ and activation of microglia, astrocyte and oligodendrocyte were examined by immunohistochemistry of TNFɑ, interginɑM(OX42), glial fibrillary acidic protein(GFAP)and myelin. Using suture occlusion technique,the right middle cerebral artery in rats was occluded. SD rats and murine TNFɑ transgenic rats were subjected to 1 hour of the right middle cerebral artery occlusion.Seventy-two hours after reperfusion,neuronal deficit scores were calculated,and infarct volume was calculated by 2,3,5-triphenyltetrazolium chloride monohydrate (TTC) staining. Results: TNFɑ overexpression and hypertrophic and proliferative changes of microglia, astrocyte and oligodendrocyte in the non-ischemia brain tissue of murine TNFɑ transgenic rats were observed. Neuronal deficit scores and infarct volume of murine TNFɑ transgenic rats for after 1 hour of occlusion and 72 hours of reperfusion were higher than those of SD rats. Conclusion: Overexpression of TNFɑ gene can activate microglia, astrocyte and oligodendrocyte in the non-ischemic brain tissue, and increase neuronal deficit scores and infarct volume significantly, which suggests that it can aggravate cerebral ischemic injury.
出处
《山东大学学报（医学版）》
CAS
2004年第5期567-570,共4页
Journal of Shandong University:Health Sciences
基金
国家自然科学基金资助课题(30270492)。
