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成年大鼠暴露于溴化乙锭后大脑中髓鞘再生的动力学

Dynamics of remyelination in the brain of adult rats after exposure to ethidium bromide.

作者信息

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

机构信息

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

出版信息

J Submicrosc Cytol Pathol. 1998 Jul;30(3):341-8.

PMID:9723194
Abstract

Diseases of the central nervous system with limited prognosis, as multiple sclerosis, have led to the development of experimental models to study the pathophysiology of such diseases. The present investigation deals with the ethidium bromide (EB) model of demyelination with the objective to study the pathogenesis of encephalic demyelinating lesions. A single 10 microliters injection of 0.1% EB in 0.15 M saline was inoculated in the ventral surface of the pons of adult Wistar rats and after times ranging from 24 h to 30 days, the animals were anaesthetized and perfused with Karnovsky fixative for light and electron microscopy studies. From 3 to 7 days after the EB injection the tissue had developed a spongiotic aspect with intra- and extracellular swelling, demyelinating fibers and a number of necrotic glial cells. By 11 days the reactive phase had begun, and a large number of macrophages had migrated to the foci of the lesion, initiating the absorption of the necrotic tissue. In addition, there were oligodendrocyte-remyelinating nerve fibers and astrocytic gliosis. At 15 days Schwann cells-remyelinating fibers were first seen at the periphery of the lesion while the central area acquired a cystic pattern. The results obtained with the EB-demyelinating model in brain of adult rats showed that 1) remyelination by oligodendrocytes surpassed that by Schwann cells and 2) astrocytic processes were present at the areas remyelinated by the former and absent from those remyelinated by the latter.

摘要

预后有限的中枢神经系统疾病,如多发性硬化症,促使了用于研究此类疾病病理生理学的实验模型的发展。本研究探讨了溴化乙锭(EB)脱髓鞘模型,旨在研究脑脱髓鞘病变的发病机制。将10微升0.1%的EB注射到成年Wistar大鼠脑桥腹侧表面的0.15 M盐水中,在24小时至30天的不同时间点后,对动物进行麻醉并用Karnovsky固定剂灌注,用于光镜和电镜研究。在EB注射后3至7天,组织出现海绵样外观,伴有细胞内和细胞外肿胀、脱髓鞘纤维以及一些坏死的神经胶质细胞。到11天时,反应期开始,大量巨噬细胞迁移到病变部位,开始吸收坏死组织。此外,有少突胶质细胞重新髓鞘化的神经纤维和星形胶质细胞增生。在15天时,首次在病变周边看到雪旺细胞重新髓鞘化的纤维,而中心区域呈现囊性结构。在成年大鼠脑中用EB脱髓鞘模型获得的结果表明:1)少突胶质细胞的重新髓鞘化超过雪旺细胞;2)在少突胶质细胞重新髓鞘化的区域有星形胶质细胞突起,而在雪旺细胞重新髓鞘化的区域则没有。

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