Polycyclic aromatic hydrocarbons in urban particle matter exacerbate movement disorder after ischemic stroke via potentiation of neuroinflammation.

IF 7.2 1区医学 Q1 TOXICOLOGY

Particle and Fibre Toxicology Pub Date : 2023-02-16 DOI:10.1186/s12989-023-00517-x

Miki Tanaka, Tomoaki Okuda, Kouichi Itoh, Nami Ishihara, Ami Oguro, Yoshiaki Fujii-Kuriyama, Yu Nabetani, Megumi Yamamoto, Christoph F A Vogel, Yasuhiro Ishihara

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引用次数: 3

Abstract

Background: A recent epidemiological study showed that air pollution is closely involved in the prognosis of ischemic stroke. We and others have reported that microglial activation in ischemic stroke plays an important role in neuronal damage. In this study, we investigated the effects of urban aerosol exposure on neuroinflammation and the prognosis of ischemic stroke using a mouse photothrombotic model.

Results: When mice were intranasally exposed to CRM28, urban aerosols collected in Beijing, China, for 7 days, microglial activation was observed in the olfactory bulb and cerebral cortex. Mice exposed to CRM28 showed increased microglial activity and exacerbation of movement disorder after ischemic stroke induction. Administration of core particles stripped of attached chemicals from CRM28 by washing showed less microglial activation and suppression of movement disorder compared with CRM28-treated groups. CRM28 exposure did not affect the prognosis of ischemic stroke in null mice for aryl hydrocarbon receptor, a polycyclic aromatic hydrocarbon (PAH) receptor. Exposure to PM2.5 collected at Yokohama, Japan also exacerbated movement disorder after ischemic stroke.

Conclusion: Particle matter in the air is involved in neuroinflammation and aggravation of the prognosis of ischemic stroke; furthermore, PAHs in the particle matter could be responsible for the prognosis exacerbation.

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城市颗粒物中的多环芳烃通过增强神经炎症加剧缺血性脑卒中后的运动障碍。

背景:最近一项流行病学研究表明，空气污染与缺血性脑卒中的预后密切相关。我们和其他人已经报道了缺血性中风中的小胶质细胞激活在神经元损伤中起重要作用。在这项研究中，我们利用小鼠光血栓模型研究了城市气溶胶暴露对缺血性卒中神经炎症和预后的影响。结果:当小鼠鼻内暴露于中国北京收集的城市气溶胶CRM28 7天时，观察到嗅球和大脑皮层的小胶质细胞活化。暴露于CRM28的小鼠在缺血性卒中诱导后显示小胶质细胞活性增加和运动障碍加剧。与CRM28处理组相比，通过洗涤从CRM28中剥离附着化学物质的核心颗粒显示出更少的小胶质细胞激活和运动障碍抑制。CRM28暴露对芳烃受体(一种多环芳烃(PAH)受体)缺失小鼠的缺血性卒中预后没有影响。暴露在日本横滨收集的PM2.5中也会加剧缺血性中风后的运动障碍。结论:空气中颗粒物参与缺血性脑卒中的神经炎症及预后的恶化;此外，颗粒物质中的多环芳烃可能是导致预后恶化的原因。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Particle and Fibre Toxicology TOXICOLOGY-

CiteScore

15.90

自引率

4.00%

发文量

审稿时长

6 months

期刊介绍： Particle and Fibre Toxicology is an online journal that is open access and peer-reviewed. It covers a range of disciplines such as material science, biomaterials, and nanomedicine, focusing on the toxicological effects of particles and fibres. The journal serves as a platform for scientific debate and communication among toxicologists and scientists from different fields who work with particle and fibre materials. The main objective of the journal is to deepen our understanding of the physico-chemical properties of particles, their potential for human exposure, and the resulting biological effects. It also addresses regulatory issues related to particle exposure in workplaces and the general environment. Moreover, the journal recognizes that there are various situations where particles can pose a toxicological threat, such as the use of old materials in new applications or the introduction of new materials altogether. By encompassing all these disciplines, Particle and Fibre Toxicology provides a comprehensive source for research in this field.