慢性实验性变应性猴脑脊髓炎的超微结构改变  

Ultrastructure of chronic experimental allergic encephalomyelitis in cynomolgus monkeys

作　　者：胡学强[1] 郭怡菁[1] 陆正齐[1] 陶拓宇[1] 吴义芳[2] 

机构地区：[1]中山大学附属第三医院神经科,广州510630 [2]中山大学医学院电镜室

出　　处：《中华神经科杂志》2002年第4期221-223,共3页Chinese Journal of Neurology

基　　金：广东省教育厅"千;百;十人才工程"基金资助项目( 9946 )

摘　　要：目的　探讨自身免疫性中枢神经系统脱髓鞘疾病慢性型的病理特点及其可能机制。方法　成功建立猴实验性变态反应性脑脊髓炎模型数年后 ,根据MR摄片结果定位病灶并作分类 ,然后进行病理取材和电镜观察超微结构。结果　 (1)活动性病灶内见成片的髓鞘松解、断裂或融合 ,轴突空泡样变性、皱缩或消失 ,少突胶质细胞变性 ,未见淋巴细胞浸润 ,仅见散在巨噬细胞 ,伴明显的间质水肿 ;(2 )可疑活动性病灶内见部分髓鞘内板松解 ,其内轴突有轻度空泡样变 ,亦见少突胶质细胞变性 ,散在巨噬细胞 ,未见淋巴细胞浸润。结论　慢性EAE的病理改变不仅有髓鞘的变性 ,同时轴突的病变也十分明显。Objective To investigate the pathological features of the chronic autoimmune demyelinating disease in central nervous system(CNS) using the experimental allergic encephalomyelitis(EAE) model in cynomolgus monkeys. Methods The EAE model were established in cynomolgus at first. Four years later, we obtained the active and indefinite active EAE tissue blocks according to the demonstration of MR, and then made observations under a electronic microscope. Results We found that (1)in the definite active lesions, most of the myelin circles were loosened, broked, or combined with each other, while the axons were transformed into vesicular networks, crimpled or even disappearing in the degenerated myelin circles; (2)in the indefinite active lesions, the pathological changes were less severe than the former; (3)in both of the two kinds of lesions, there were no permeance of lymphocytes. Conclusion Are there not only degenerations of myelin in the chronic EAE lesions, but also remarkable changes of axons.

关 键 词：脑脊髓炎 自身免疫性 多发性硬化 超微结构 发病机制 脱髓鞘性疾病 

分 类 号：R744.3[医药卫生—神经病学与精神病学]