暴露于空气污染纳米颗粒:氧化应激和神经炎症

M. Ehsanifar, Banihashemian Ss, Masoud Ehsanifar
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引用次数: 4

摘要

城市空气污染物暴露被认为是导致中枢神经系统(CNS)和神经病理学疾病的神经炎症和氧化应激的来源。过渡金属、颗粒物(PM),包括PM 2.5 (PM <2.5 μm)和PM 0.1 (PM <0.1μm)、氮氧化物和臭氧是能够产生活性氧(ROS)的有效氧化剂。氧化应激可引起氧化还原敏感通路,导致各种生物过程,包括炎症和细胞死亡。阿尔茨海默病(AD)和帕金森病(PD)以及中风的发病率与暴露于空气污染有关。最近的一些研究结果表明,城市空气污染物除了会导致肺部和心血管疾病外,还会影响大脑,并影响中枢神经系统的健康。虽然潜在的CNS病理机制诱导空气污染物暴露尚不清楚,但最近的研究表明,血脑屏障(BBB)和小胶质细胞激活的变化是关键组成部分。在这项工作中,我们回顾了环境空气污染到达大脑并激活先天免疫反应作为氧化应激和神经炎症因子来源的机制的新证据。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Exposure to Air Pollution Nanoparticles: Oxidative Stress and Neuroinflammation
Urban air pollutants exposure is known as a source of neuroinflammation and oxidative stress that causes the Central Nervous System (CNS) and neuropathology disease. Transition metals, Particulate Matter (PM), including PM 2.5 (PM <2.5 μm) and PM 0.1 (PM <0.1μm), nitrogen oxides and ozone are of potent or oxidant capable of producing Reactive Oxygen Species (ROS). Redox-sensitive pathways can be caused by oxidative stress, leading to various biological processes, including inflammation and cell death. The incidence of Alzheimer's Disease (AD) and Parkinson's Disease (PD) and stroke are associated with exposure to air pollution. Some recent findings suggest that urban air pollutants reach the brain in addition to pulmonary and cardiovascular diseases and affect the CNS health too. While the underlying CNS pathology mechanisms induced air pollutants exposure are not well understood, recent studies show that changes in Blood Brain Barrier (BBB) and microglial activation are key components. In this work, we reviewed the new evidence of the mechanisms by which ambient air pollution reach the brain and activate innate immune response as a source of oxidative stress and neuroinflammatory factors.
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