在小鼠中的聚烯,聚烯和聚乙烯微塑料碎片的肺毒性评估
Isaac Kwabena Danso1,2, Jong-Hwan Woo1,3, Seung Hoon Baek1,2
1Inhalation Toxicology Center for Airborne Risk Factor, Korea Institute of Toxicology, 30 Baehak1-Gil, Jeongeup, Jeollabuk-do 56212 Republic of Korea.
Toxicological research
|March 25, 2024
概括
聚乙烯微塑料通过激活TLR4通路,触发小鼠的肺炎,导致NF-κB和NLRP3炎症酶反应. 聚烯和聚乙烯微塑料没有引起显著的炎症效应.
科学领域:
- 环境健康 环境健康
- 毒理学 毒理学 毒理学
- 肺部医学 肺部医学
背景情况:
- 像聚烯 (PP),聚烯 (PS) 和聚乙烯 (PE) 这样的普通家用材料的微塑料在室内空气中普遍存在.
- 人们越来越担心可吸入微塑料对呼吸系统健康的影响,特别是在COVID-19大流行期间室内时间增加之后.
- 不同类型的微塑料对肺系统的特定毒理影响仍然不完全理解.
研究的目的:
- 在小鼠模型中研究PP,PS和PE微塑料碎片的肺毒性.
- 阐明微塑料诱导的肺炎背后的分子机制.
主要方法:
- 在C57BL/6小鼠的实验中,小鼠每天在14天内内心灌注5mg/kg的PP,PS或PE微塑料.
- 支气管洗液 (BALF) 和肺组织分析了炎症细胞数量,细胞因子/化学因子水平以及关键信号通路蛋白质.
- 评估的是托尔类受体 (TLR) 表达,核因子kappa B (NF-κB) 激活,以及NLRP3炎症组分水平.
主要成果:
- 与对照人群相比,PS微塑料灌注显著增加了BALF中的炎症细胞 (巨细胞,中性粒细胞,乙蛋白细胞) 和炎症介质.
- 暴露于PS导致TLR4蛋白水平升高,激活NF-κB信号传递,以及肺组织中NLRP3炎症组分 (NLRP3,ASC,Caspase-1) 的增加.
- 与载体对照组相比,PP和PE微塑料没有诱导显著的炎症反应或改变测量的分子通路.
结论:
- 聚钢 (PS) 微塑料碎片在小鼠中诱导显著的肺炎.
- 对PS的炎症反应由托尔样受体4 (TLR4) 激活介导,导致下游NF-κB和NLRP3炎症酶途径的参与.
- 聚烯 (PP) 和聚乙烯 (PE) 微塑料在本研究中没有引起类似的炎症效应.
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