摘要
目的探讨自身免疫性中枢神经系统（ＣＮＳ）脱髓鞘的病理特点和发病过程。方法建立猴实验性变态反应性脑脊髓炎（ＥＡＥ）的模型，并从病情不同阶段进行病理取材和电镜观察。结果（１）ＥＡＥ脱髓鞘最早的靶是少突胶质细胞（ＯＤＣ），而不是髓鞘本身；（２）无论急性期还是慢性期，脱髓鞘病灶内只有极少的炎细胞浸入；（３）急性期髓鞘改变轻微，以变性为主，ＯＤＣ肿胀显著，轴突相对完整。远离髓鞘变性区有大量炎细胞浸入；（４）慢性期病变区髓鞘脱失明显，ＯＤＣ严重变性或部分丢失，继发性轴突变性，边缘可见少量薄的髓鞘再生，血脑屏障破坏。结论ＥＡＥ的ＣＮＳ脱髓鞘过程首先累及ＯＤＣ。
Objective To investigate the pathological features and the initiating factor of autoimmune CNS demyelinating diseases. Methods The animal models of experimental allergic encephalomyelitis (EAE) in cynomolgus monkeys were established. Following, two EAE animals respectively during the acute and chronic stages were killed, and a healthy monkey was killed, too. Numerous brain blocks was obtained from the above mentiond three animals and the observations were made under an electron microscope. Results The findings demonstrated that (1) the first target attacked by the immune events was oligodendrocytes, but not the myelin sheaths itself: (2) during the acute stage or chronic stage, in the demyelinating plaques, there were only a few inflammentory, cells infiltration; (3) in the acute stage, the myelin sheaths were markedly loosen and the axon myelins seperated, but the axons were relatively perserved and in the patch away from the degenerated myelin there were a number of inflammentory cellular infiltrations; (4) in chronic lesions, myelin sheath loss was obvious, secondary axonal injuries was severe, including axon swelling and loss with oligodendrocytes markedly reduced or degenerated, but there were fewest in flammentory cells seen at the edge of the lesions with thin remyelination and persistently damaged blood brain barrier. Conclusion Our studies indicated that the demyelinating process of EAE possibely involved the oligodendrocytes primarily.
出处
《中华神经科杂志》
CAS
CSCD
1998年第6期333-335,共3页
Chinese Journal of Neurology
基金
国家自然科学基金
国家教委博士点基金
关键词
食蟹猴
脑脊髓炎
病理
超微结构
Cynomolgus Experimental allergic encephalomyelitis Multiple sclerosis Ultrastructure
