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作者

Haiyun Wei, Chao Chen, Fanglin Di, Changhua Sun, Xinzhi Wang, Meng Sun, Natong Liu, Min Zhang, Meng Li, Jie Zhang, Shuping Zhang, Xue Liang

作者单位

Biomedical Sciences College & Shandong Medicinal Biotechnology Centre, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong, 250117, China. ⁷ School of Public Health, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong, 250117, China Medical Science and Technology Innovation Center, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong, 250117, China. ² Biomedical Sciences College & Shandong Medicinal Biotechnology Centre, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong, 250117, China. ³ Shandong Center for Disease Control and Prevention, Jinan, Shandong, 250014, China. ⁴ School of Public Health, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong, 250117, China. ⁵ Department of Neurosurgery, The First Affiliated Hospital of Shandong First Medical University, Jinan, Shandong, 250014, China. ⁶ Medical Science and Technology Innovation Center, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong, 250117, China Medical Science and Technology Innovation Center, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong, 250117, China. Electronic address: liangxue@sdfmu.edu.cn. Affiliations ¹ School of Public Health, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong, 250117, China

刊名

Environmental pollution (Barking, Essex : 1987)

年份

2024

卷号

Vol.352

页码

124130

ISSN

1873-6424

关键词

Ferroptosis Fine particulate matter Heme oxygenase-1 Inflammation Microglia.

摘要

Particulate matter has been a dominant contributor to air contamination, which will enter the central nervous system , causing neurotoxicity. However, the biological mechanism is poorly identified. In this study, C57BL/6J mice were applied to evaluate the neurotoxicity of collected fine particulate matter , via oropharyngeal aspiration at two ambient equivalent concentrations. The Y-maze results showed that PM exposure in mice would lead to the damage in hippocampal-dependent working memory. In...更多

Particulate matter has been a dominant contributor to air contamination, which will enter the central nervous system , causing neurotoxicity. However, the biological mechanism is poorly identified. In this study, C57BL/6J mice were applied to evaluate the neurotoxicity of collected fine particulate matter , via oropharyngeal aspiration at two ambient equivalent concentrations. The Y-maze results showed that PM exposure in mice would lead to the damage in hippocampal-dependent working memory. In addition, cell neuroinflammation, microglial activation were detected in hippocampus of PM-exposure mice. To confirm the underlying mechanism, the microarray assay was conducted to screen the differentially expressed genes in microglia after PM exposure, and the results indicated the enrichment of DEGs in ferroptosis pathways. Furthermore, Heme oxygenase-1 was found to be one of the most remarkably upregulated genes after PM exposure for 24 h. And PM exposure induced ferroptosis with iron accumulation through heme degradation by Nrf2-mediated Hmox1 upregulation, which could be eliminated by Nrf2-inhibition. Meanwhile, Hmox1 antagonist zinc protoporphyrin IX could protect BV2 cells from ferroptosis. The results taken together indicated that PM resulted in the ferroptosis by causing iron overload through Nrf2/Hmox1 signaling pathway, which could account for the inflammation in microglia.收起

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