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载脂蛋白A-I在多发性硬化症发病机制中的作用。

A role for Apolipoprotein A-I in the pathogenesis of multiple sclerosis.

作者信息

Meyers Lindsay, Groover Chassidy J, Douglas Joshua, Lee Sangmin, Brand David, Levin Michael C, Gardner Lidia A

机构信息

Research Service VAMC, Memphis, TN 38104, United States.

Research Service VAMC, Memphis, TN 38104, United States; Department of Neurology, University of Tennessee Health Science Center, Memphis, TN 38163, United States.

出版信息

J Neuroimmunol. 2014 Dec 15;277(1-2):176-85. doi: 10.1016/j.jneuroim.2014.10.010. Epub 2014 Oct 30.

Abstract

Apolipoprotein A1 (Apo A-I), the most abundant component of high-density lipoprotein (HDL), is an anti-inflammatory molecule, yet its potential role in the pathogenesis of multiple sclerosis (MS) has not been fully investigated. In this study, Western blot analyses of human plasma showed differential Apo A-I expression in healthy controls compared to MS patients. Further, primary progressive MS patients had less plasma Apo A-I than other forms of MS. Using experimental allergic encephalomyelitis (EAE) as a model for MS, Apo A-I deficient mice exhibited worse clinical disease and more neurodegeneration concurrent with increased levels of pro-inflammatory cytokines compared to wild-type animals. These data suggest that Apo A-I plays a role in the pathogenesis of EAE, a model for MS, creating the possibility for agents that increase Apo A-I levels as potential therapies for MS.

摘要

载脂蛋白A1(Apo A-I)是高密度脂蛋白(HDL)中含量最丰富的成分,是一种抗炎分子,但其在多发性硬化症(MS)发病机制中的潜在作用尚未得到充分研究。在本研究中,对人血浆进行的蛋白质印迹分析显示,与MS患者相比,健康对照中Apo A-I的表达存在差异。此外,原发性进行性MS患者的血浆Apo A-I水平低于其他形式的MS患者。使用实验性自身免疫性脑脊髓炎(EAE)作为MS的模型,与野生型动物相比,Apo A-I缺陷小鼠表现出更严重的临床疾病和更多的神经退行性变,同时促炎细胞因子水平升高。这些数据表明,Apo A-I在EAE(一种MS模型)的发病机制中起作用,这为增加Apo A-I水平的药物作为MS的潜在治疗方法创造了可能性。

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