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暴露于细颗粒物(PM)会阻碍髓鞘修复在一个脱髓鞘的小鼠模型中的作用。

Exposure to fine particulate matter (PM) hampers myelin repair in a mouse model of white matter demyelination.

机构信息

Department of Neuroscience Rita Levi-Montalcini, University of Turin, Italy; Neuroscience Institute Cavalieri Ottolenghi (NICO), University of Turin, Regione Gonzole, 10, 10043, Orbassano (Turin), Italy.

Neuroscience Institute Cavalieri Ottolenghi (NICO), University of Turin, Regione Gonzole, 10, 10043, Orbassano (Turin), Italy; Neurobiology Unit, Neurology-CReSM (Regional Referring Center of Multiple Sclerosis), AOU San Luigi Gonzaga, Regione Gonzole 10, 10043, Orbassano, Italy; Department of Molecular Biotechnology and Health Sciences, University of Turin, via Nizza 52, 10126, Turin, Italy.

出版信息

Neurochem Int. 2021 May;145:104991. doi: 10.1016/j.neuint.2021.104991. Epub 2021 Feb 12.

Abstract

Epidemiological studies show a strong association between exposure to air pollution - and particularly to particulate matter (PM) -, increased prevalence of Multiple Sclerosis (MS) and higher rates of hospital admissions for MS and MS relapses. Besides having immunomodulatory effects and sustaining a systemic oxidative-inflammatory response, PM may participate in MS pathogenesis by targeting also Central Nervous System (CNS)-specific processes, such as myelin repair. Here we show that, in a mouse model of lysolecithin-induced demyelination of the subcortical white matter, post-injury exposure to fine PM hampers remyelination, disturbs oligodendroglia differentiation dynamics and promotes astroglia and microglia reactivity. These findings support the view that exposure to fine PM can contribute to demyelinating pathologies by targeting the endogenous regenerative capability of the CNS tissue.

摘要

流行病学研究表明,暴露于空气污染 - 特别是颗粒物 (PM) - 与多发性硬化症 (MS) 的患病率增加以及 MS 住院和 MS 复发率升高之间存在很强的关联。除了具有免疫调节作用和维持系统性氧化炎症反应外,PM 还可能通过靶向中枢神经系统 (CNS) 特异性过程,如髓鞘修复,参与 MS 的发病机制。在这里,我们表明,在亚皮质白质中由溶血卵磷脂诱导脱髓鞘的小鼠模型中,损伤后暴露于细颗粒物会阻碍髓鞘再生,扰乱少突胶质细胞分化动力学,并促进星形胶质细胞和小胶质细胞的反应性。这些发现支持这样一种观点,即暴露于细颗粒物可能通过靶向中枢神经系统组织的内源性再生能力而导致脱髓鞘病变。

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