摘要
目的:动态观察核因子-κB(NF-κB)及胶质纤堆酸性蛋白(GFAP)在外伤性癫痫(PTE)模型皮层或海马的表达, 探讨有关发病机制。方法:立体定向注射1000 nmol FeCl2于大鼠右侧运动皮层致痫。在不同时间点行为学视频、脑电图监测,皮层或海马行HE染色、普鲁士蓝和腾氏蓝反应、抗GFAP及抗NF-κB二重免疫荧光组织化学方法结合激光共聚焦显微镜行病理学观察。结果:所有大鼠在注射FeCl2后不久记录到癫痫样放电。致痫后1h即可见皮层和海马神经元 NF-κB大量表达,7d后减少;而皮层和海马胶质细胞NF—κB在7d后可见移至核内,30 d后明显减少; GFAP在7～14 d后表达增强;在7 d见到较多的NF-κB及GFAP双标阳性胶质细胞。结论:FeCl2皮层注射可以制成PTE动物模型。与NF-κB表达相关的神经元及胶质细胞的动态变化在PTE的发病机制中起重要作用。NF-κB表达增加可能为FeCl2 致痫的共同途径。
Objective：To observe the kinesis expression of NF-kB and GFAP in the cortex and Hippocampus,and discuss the mechanism of pathologic changes and epileptogenesis in the model of posttraumatic epilepsy （PTE）. Methods： Ferrous chloride （FeCl2,1000 nmol） was injected into the motor cortex of rats via stereotactic technique. Behavior was observed and EEG were recorded following injection. The pathologic examination was performed,including HE, Perls blue, Turnbull blue staining. The NF-kB and GFAP expression in the cortex and Hippocampus detected by immunofluorescenee staining with Laser confocal scanning microscope. Results： All of the rats developed epileptiform discharges soon after FeCl2 --injection. Compared with the control group, the expression of NF-kB were increased in 1 hour, decreased in 7 days later, decreased significantly in 30 days later; the expression of GFAP were increased in 7 or 14 days later, and there were no significance in 14 and 21 or 30 days later. There are some neurons and glia expressing NF-kB and GFAP at the same time. Conclusion： The intracortieal injection of 1000nmol FeCl2 induced model is an ideal animal PTE model. The changes of the kinesis expression of NF-kB and GFAP in the cortex and Hippocampus concerned with the mechanism of pathologic changes and epileptogenesis in this model.
出处
《中国临床医学》
北大核心
2006年第2期188-190,共3页
Chinese Journal of Clinical Medicine
基金
军队十五重大临床技术项目(2002卫医字18-16号)
