Complement 3-deficient mice are not protected against MPTP-induced dopaminergic neurotoxicity
Complement 3-deficient mice are not protected against MPTP-induced dopaminergic neurotoxicity
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DOI：
10.1016/j.brainres.2007.08.033
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发表时间：
2007-10-31
期刊：
影响因子：
2.9
通讯作者：
Su, Bingyin
中科院分区：
文献类型：
--
作者：
Liang, Yajie;Li, Shurong;Su, Bingyin
最近的研究表明，炎症是帕金森氏病(PD)发病的主要因素。新的证据表明，补体系统的组成部分可能参与了这种紊乱，并促进了它的发展。因此，我们观察了补体系统的关键成分补体3(C3)缺乏对急性或慢性给予1-甲基-4-苯基-1，2，3，6-四氢吡啶(MPTP)所致黑质致密质(SNPC)多巴胺能神经元死亡和纹状体多巴胺能纤维丢失的影响。SNPC多巴胺能神经元免疫组织化学染色和纹状体多巴胺及其代谢物的神经化学分析显示，两种基因型间的差异无统计学意义。较长的存活时间也表明C3可能不介导MPTP急性攻击的小鼠纹状体多巴胺能纤维的自发恢复。我们的结论是，尽管越来越多的证据表明补体系统参与了帕金森病的发病机制，但我们的数据并不支持C3在这种已建立的帕金森病模型中的作用，正如高效液相分析和免疫组织化学染色的结果所表明的那样。(C)2007 Elsevier B.V.保留所有权利。
Recent studies have invoked inflammation as a major contributor to the pathogenesis of Parkinson's disease (PD). Emerging evidence indicated that components of complement system may be involved in such disorder and contribute to its development. We thus observed the influence of deficiency of complement 3 (C3), the key component of complement system, on the death of dopaminergic neurons in substantia nigra pays compacta (SNpc) and the loss of dopaminergic fibers in striatum induced by acute or chronic administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Immunohistochemical staining of dopaminergic neurons in SNpc and neurochemical analysis of dopamine and its metabolites in striata revealed that there was no significant difference between the two genotypes. Longer survival time also indicated that C3 might not mediate the spontaneous recovery of dopaminergic fibers in mouse striaturn acutely challenged by MPTP. We conclude that, despite growing evidence indicating the involvement of complement system in the pathogenesis of PD, our data do not support a role for C3 in this established model of PD, as indicated by results from HPLC analysis and immunohistochemical staining. (C) 2007 Elsevier B.V. All rights reserved.