School of Respiratory Therapy, College of Medicine, Taipei Medical University, Taipei, Taiwan; Division of Pulmonary Medicine, Department of Internal Medicine, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan; Division of Pulmonary Medicine Department of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
School of Public Health, College of Public Health, Taipei Medical University, Taipei, Taiwan; Department of Public Health, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Environ Toxicol Pharmacol. 2018 Sep;62:54-59. doi: 10.1016/j.etap.2018.06.007. Epub 2018 Jun 22.
Particulate air pollution is recognized as a potential risk factor for neurological disorders; however, the underlying mechanisms of neurodegenerative diseases that occur due to particulate air pollution remain unclear. The objective of the present study was to evaluate the neurotoxic effects caused by diesel exhaust particles (DEPs). We determined the ability of DEPs and carbon black (CB) to induce neurotoxicity, oxidative stress and inflammation, and to disrupt the expression of tau and autophagy proteins in human neuroblastoma IMR-32 cells. Spherical CB (dominated by C, N, and S) and DEPs (dominated by C, N, and O) in aggregates were observed using a field emission-scanning electron microscope (FE-SEM) equipped with energy-dispersive x-ray (EDX) microanalysis. Cell viability was significantly decreased by CB and DEPs in IMR-32 cells, but neither particle altered malondialdehyde (MDA) production. We observed that exposure to DEPs significantly increased 8-isoprostane and tumor necrosis factor (TNF)-α levels. Significantly increased expression of tau was induced in IMR-32 cells by DEPs but not by CB. Expression of beclin 1 was increased by DEPs, whereas the light chain 3II (LC3II)/LC3I ratio was increased by CB. Results of the present study suggested that DEPs induced neuroinflammation, oxidative stress, and neurodegenerative-related tau overexpression and regulation by autophagy in IMR-32 cells. We demonstrated that DEPs are able to induce neurotoxicity, which could be associated with the development of neurodegenerative diseases.
颗粒物空气污染被认为是神经紊乱的潜在风险因素；然而，由于颗粒物空气污染而导致的神经退行性疾病的潜在机制仍不清楚。本研究的目的是评估柴油机排气颗粒（DEPs）引起的神经毒性作用。我们测定了 DEPs 和炭黑（CB）诱导神经毒性、氧化应激和炎症的能力，并测定了它们对人神经母细胞瘤 IMR-32 细胞中 tau 和自噬蛋白表达的干扰作用。场发射扫描电子显微镜（FE-SEM）配备能量色散 X 射线（EDX）微分析，观察到聚集的球形 CB（以 C、N 和 S 为主）和 DEPs（以 C、N 和 O 为主）。CB 和 DEPs 使 IMR-32 细胞中的细胞活力显著降低，但两种颗粒均未改变丙二醛（MDA）的产生。我们观察到 DEPs 暴露使 8-异前列腺素和肿瘤坏死因子（TNF）-α水平显著增加。DEPs 显著诱导 IMR-32 细胞中的 tau 表达增加，但 CB 则没有。DEPs 增加了 beclin 1 的表达，而 CB 则增加了 LC3II/LC3I 的比值。本研究的结果表明，DEPs 诱导了 IMR-32 细胞中的神经炎症、氧化应激和神经退行性相关的 tau 过表达以及自噬的调节。我们证明 DEPs 能够诱导神经毒性，这可能与神经退行性疾病的发生有关。
