Effects of diesel exhaust particles on the expression of tau and autophagy proteins in human neuroblastoma cells

Kuan Jen Bai, Kai Jen Chuang, Sheng Ming Wu, Li Te Chang, Ta Yuan Chang, Kin Fai Ho, Hsiao Chi Chuang

研究成果: 雜誌貢獻文章

4 引文 斯高帕斯(Scopus)

摘要

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.
原文英語
頁(從 - 到)54-59
頁數6
期刊Environmental Toxicology and Pharmacology
62
DOIs
出版狀態已發佈 - 九月 1 2018

ASJC Scopus subject areas

  • Toxicology
  • Pharmacology
  • Health, Toxicology and Mutagenesis

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