Mozaffari Shilan, Hassanvand Mohammad Sadegh, Baeeri Maryam, Gholami Mahdi, Bayrami Zahra, Yunesian Masud, Sahraian Mohammad Ali, Nikfar Shekoufeh, Abdollahi Mohammad
Department of Toxicology and Pharmacology, Faculty of Pharmacy and Pharmaceutical Sciences Research Center (PSRC), Tehran University of Medical Sciences, Tehran, Iran.
Department of Environmental Health Engineering, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
Toxicol Mech Methods. 2025 Jul;35(6):581-591. doi: 10.1080/15376516.2025.2468726. Epub 2025 Mar 11.
There is mounting evidence about the connection between particulate matter (PM) and neuroinflammation. This study aimed to evaluate the toxicological effects of PM associated with inflammatory factors in a mouse's multiple sclerosis (MS) model. Thirty C57BL/6 male mice were categorized into five groups: a group of healthy mice, a control cuprizone-induced MS group, and three MS-induced groups, intranasally exposed to three concentrations of ambient air PM (5, 10, and 20 mg/mL) from Tehran in a phosphate-buffered saline (PBS) solution. All mice were investigated by motor function, molecular, and histopathological assays. Moreover, the chemical content of the collected PM was assessed and reported. The cumulative exposure doses were equal to 0.025, 0.05, and 0.1 mg per gram of body weight of mice, which were approximately 3.52, 7.04, and 14.08 times higher than the human daily dose in Tehran. The PM-exposed groups showed a high inflammatory response characterized by a significant increase in the mRNA expression of tumor necrosis alpha (TNF-α), NLRP3, and interleukin 18 (IL-18). In addition, the PM-exposed groups exhibited a notably lower velocity level, total traveled distance (TD), and duration traveled in the central zone (DC) than the control group. The histopathological assays revealed significant pathological alterations and demyelination in the PM2.5-exposed groups compared to the control group. Identifying the risks and reducing the likelihood of exposure through preventive measures and regulations can result in financial savings and improve the quality of life for MS patients.
越来越多的证据表明颗粒物（PM）与神经炎症之间存在关联。本研究旨在评估在小鼠多发性硬化症（MS）模型中，与炎症因子相关的PM的毒理学效应。将30只C57BL/6雄性小鼠分为五组：一组健康小鼠、一组对照性铜螯合剂诱导的MS组以及三组诱导性MS组，通过鼻腔给予磷酸盐缓冲盐水（PBS）溶液中来自德黑兰的三种浓度（5、10和20mg/mL）的环境空气PM。通过运动功能、分子和组织病理学检测对所有小鼠进行研究。此外，还对收集到的PM的化学成分进行了评估和报告。累积暴露剂量分别等于每克小鼠体重0.025、0.05和0.1mg，分别约为德黑兰人类每日剂量的3.52、7.04和14.08倍。暴露于PM的组表现出高度炎症反应，其特征为肿瘤坏死因子α（TNF-α）、NLRP3和白细胞介素18（IL-18）的mRNA表达显著增加。此外，与对照组相比，暴露于PM的组在速度水平、总行进距离（TD）和在中央区域行进的持续时间（DC）方面均显著降低。组织病理学检测显示，与对照组相比，暴露于PM2.5的组存在明显的病理改变和脱髓鞘现象。识别风险并通过预防措施和法规降低暴露可能性，可为MS患者节省资金并改善生活质量。
