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中枢神经系统脱髓鞘病变修复的生物学:一项评估。

Biology of the repair of central nervous system demyelinated lesions: an appraisal.

作者信息

Peireira L A, Cruz-Höfling M A, Dertkigil M S, Graça D L

机构信息

Department of Histology and Embryology, State University of Campinas, Brazil.

出版信息

Arq Neuropsiquiatr. 1996 Jun;54(2):331-4. doi: 10.1590/s0004-282x1996000200026.

DOI:10.1590/s0004-282x1996000200026
PMID:8984997
Abstract

The integrity of myelin sheaths is maintained by oligodendrocytes and Schwann cells respectively in the central nervous system (CNS) and in the peripheral nervous system. The process of demyelination consisting of the withdrawal of myelin sheaths from their axons is a characteristic feature of multiple sclerosis, the most common human demyelinating disease. Many experimental models have been designed to study the biology of demyelination and remyelination (repair of the lost myelin) in the CNS, due to the difficulties in studying human material. In the ethidium bromide (an intercalating gliotoxic drug) model of demyelination, CNS remyelination may be carried out by surviving oligodendrocytes and/or by cells differentiated from the primitive cell lines or either by Schwann cells that invade the CNS. However, some factors such as the age of the experimental animals, intensity and time of exposure to the intercalating chemical and the topography of the lesions have marked influence on the repair of the tissue.

摘要

在中枢神经系统(CNS)和外周神经系统中,髓鞘的完整性分别由少突胶质细胞和施万细胞维持。脱髓鞘过程,即髓鞘从轴突上脱离,是多发性硬化症(最常见的人类脱髓鞘疾病)的一个特征。由于研究人体材料存在困难,人们设计了许多实验模型来研究中枢神经系统中脱髓鞘和髓鞘再生(修复丢失的髓鞘)的生物学过程。在溴化乙锭(一种嵌入性神经毒性药物)脱髓鞘模型中,中枢神经系统的髓鞘再生可能由存活的少突胶质细胞和/或从原始细胞系分化而来的细胞进行,或者由侵入中枢神经系统的施万细胞进行。然而,一些因素,如实验动物的年龄、接触嵌入性化学物质的强度和时间以及病变的部位,对组织修复有显著影响。

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