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胶质细胞在神经毒素诱导的帕金森病动物模型中的作用。

Role of glial cells in neurotoxin-induced animal models of Parkinson's disease.

机构信息

Department of Neurobiology and Therapeutics, Graduate School and Faculty of Pharmaceutical Sciences, The University of Tokushima, 1-78, Sho-machi, Tokushima, 770-8505, Japan.

出版信息

Neurol Sci. 2011 Feb;32(1):1-7. doi: 10.1007/s10072-010-0424-0. Epub 2010 Nov 24.

Abstract

Dopaminergic neurons are selectively vulnerable to oxidative stress and inflammatory attack. The neuronal cell loss in the substantia nigra is associated with a glial response composed markedly of activated microglia and, to a lesser extent, of reactive astrocytes although these glial responses may be the source of neurotrophic factors and can protect against oxidative stress such as reactive oxygen species and reactive nitrogen species. However, the glial response can also mediate a variety of deleterious events related to the production of pro-inflammatory, pro-oxidant reactive species, prostaglandins, cytokines, and so on. In this review, we discuss the possible protective and deleterious effects of glial cells in the neurodegenerative diseases and examine how these factors may contribute to the pathogenesis of Parkinson's disease. This review suggests that further investigation concerning glial reaction in Parkinson's disease may lead to disease-modifying therapeutic approaches and may contribute to the pathogenesis of this disease.

摘要

多巴胺能神经元易受氧化应激和炎症攻击。黑质中的神经元丧失与由激活的小胶质细胞组成的明显的神经胶质反应有关,并且在较小程度上与反应性星形胶质细胞有关,尽管这些神经胶质反应可能是神经营养因子的来源并且可以抵抗氧化应激,例如活性氧和活性氮。然而,神经胶质反应也可以介导与产生促炎、促氧化剂反应性物质、前列腺素、细胞因子等相关的多种有害事件。在这篇综述中,我们讨论了神经胶质细胞在神经退行性疾病中的可能保护和有害作用,并研究了这些因素如何导致帕金森病的发病机制。这篇综述表明,进一步研究帕金森病中的神经胶质反应可能会导致疾病修饰的治疗方法,并有助于该疾病的发病机制。

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