Liu Xin-Qi, Huang Jia, Song Chao, Zhang Tian-Liang, Liu Yong-Ping, Yu Li
School of Basic Medicine, Neurologic Disorders and Regenerative Repair Lab of Shandong Higher Education, Weifang Medical University, Weifang, China.
Hum Exp Toxicol. 2023 Jan-Dec;42:9603271231191436. doi: 10.1177/09603271231191436.
Recent extensive evidence suggests that ambient fine particulate matter (PM2.5, with an aerodynamic diameter ≤2.5 μm) may be neurotoxic to the brain and cause central nervous system damage, contributing to neurodevelopmental disorders, such as autism spectrum disorders, neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease, and mental disorders, such as schizophrenia, depression, and bipolar disorder. PM2.5 can enter the brain via various pathways, including the blood-brain barrier, olfactory system, and gut-brain axis, leading to adverse effects on the CNS. Studies in humans and animals have revealed that PM2.5-mediated mechanisms, including neuroinflammation, oxidative stress, systemic inflammation, and gut flora dysbiosis, play a crucial role in CNS damage. Additionally, PM2.5 exposure can induce epigenetic alterations, such as hypomethylation of DNA, which may contribute to the pathogenesis of some CNS damage. Through literature analysis, we suggest that promising therapeutic targets for alleviating PM2.5-induced neurological damage include inhibiting microglia overactivation, regulating gut microbiota with antibiotics, and targeting signaling pathways, such as PKA/CREB/BDNF and WNT/β-catenin. Additionally, several studies have observed an association between PM2.5 exposure and epigenetic changes in neuropsychiatric disorders. This review summarizes and discusses the association between PM2.5 exposure and CNS damage, including the possible mechanisms by which PM2.5 causes neurotoxicity.
最近大量证据表明，环境细颗粒物（PM2.5，空气动力学直径≤2.5μm）可能对大脑具有神经毒性并导致中枢神经系统损伤，引发神经发育障碍，如自闭症谱系障碍；神经退行性疾病，如阿尔茨海默病和帕金森病；以及精神障碍，如精神分裂症、抑郁症和双相情感障碍。PM2.5可通过多种途径进入大脑，包括血脑屏障、嗅觉系统和肠脑轴，从而对中枢神经系统产生不利影响。对人类和动物的研究表明，PM2.5介导的机制，包括神经炎症、氧化应激、全身炎症和肠道菌群失调，在中枢神经系统损伤中起关键作用。此外，接触PM2.5可诱导表观遗传改变，如DNA低甲基化，这可能导致某些中枢神经系统损伤的发病机制。通过文献分析，我们认为缓解PM2.5诱导的神经损伤的有前景的治疗靶点包括抑制小胶质细胞过度活化、用抗生素调节肠道微生物群以及靶向信号通路，如PKA/CREB/BDNF和WNT/β-连环蛋白。此外，多项研究观察到PM2.5暴露与神经精神疾病中的表观遗传变化之间存在关联。本综述总结并讨论了PM2.5暴露与中枢神经系统损伤之间的关联，包括PM2.5导致神经毒性的可能机制。
