大气颗粒物的神经毒性效应
Neurotoxic effects of airborne inhaled particulate matters
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摘要:
越来越多的流行病学和实验研究结果表明，大气颗粒物暴露诱发神经炎性反应，干扰神经突触生理，减少神经递质表达，影响脑血管功能，与阿尔茨海默病和帕金森病等神经退行性疾病的发生和发展密切相关。本文主要简述了吸入颗粒物进入神经系统的途径：鼻黏膜-嗅神经轴突-嗅球途径和体循环-血脑屏障途径。人群和动物的研究表明，吸入颗粒物的粒径和化学组成与其神经毒性效应密切相关。颗粒物诱导的神经性炎症、血脑屏障损伤和氧化应激是中枢神经系统损伤的主要发病机制。其中，颗粒物激活小胶质细胞和星形胶质细胞释放的细胞因子和活性氧自由基在神经退行性疾病的发病中发挥着重要作用。因此，未来有必要深入研究颗粒物的神经摄入机制及其毒性组分的分子作用机制。
Abstract: Cumulated epidemiological and experimental studies have demonstrated that exposure to airborne particulate matters (PM) contributes to induction of neuroinflammation, disruption of neurosynaptic physiology, reduced expression of neurotransmitters, and cerebrovascular damage, and is associated with the risk of neurodegenerative diseases including Alzheimer's and Parkinson's diseases. The review briefly described how inhaled PM are transported into the brain:through the nasal mucosa-olfactory nerve axon-olfactory bulb pathway or the systemic circulation-blood brain barrier (BBB) pathway. Human and animal studies have documented that that the particle size and chemical composition of transported PM contribute to neurotoxicity. Moreover, the mechanisms of PM affecting the central nervous system can be ascribed to increased neuroinflammation, BBB damage, and oxidative stress. Especially, microglia and astroglia have been identified as prominent sources of cytokines and reactive oxygen species to trigger neurodegenerative diseases in response to PM exposure. Therefore, future research is required to reveal the critical mechanism of PM uptake by nerve and underlying molecular mechanism of chemical components.
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