同时暴露于聚乙烯微塑料和二2-乙烯基甲酸盐会通过TRPA1-p38 MAPK通路加剧过敏性喘
Qi Han1, Xiao Gao1, Shuwei Wang1
1Hubei Key Laboratory of Genetic Regulation and Integrative Biology, School of Life Sciences, Central China Normal University, Wuhan 430079, Hubei, China.
Toxicology letters
|July 27, 2023
概括
暴露于微塑料 (MPs) 和二-2-乙烯基) 甲酸盐 (DEHP) 共同会使过敏性喘恶化. 这种组合通过激活特定的分子通路来增加氧化应激和炎症,导致更严重的症状.
科学领域:
- 环境健康 环境健康
- 毒理学 毒理学 毒理学
- 免疫学 免疫学 免疫学
背景情况:
- 微塑料 (MP) 污染对人类健康造成越来越大的关注.
- 对于MPs和甲酸盐 (如二-2-乙烯基) 甲酸盐 (DEHP) 对过敏性喘的综合作用尚不清楚.
研究的目的:
- 研究暴露于单独或与DEHP一起的聚烯微塑料 (PS-MPs) 如何影响过敏喘.
- 阐明这些效应背后的分子机制.
主要方法:
- 在小鼠中使用卵胺 (OVA) 开发了一种过敏喘模型.
- 在28天的时间里,小鼠接受了PS-MPs (5 mg/kg bw/day) 与DEHP (0.5,5 mg/kg bw/day) 或没有DEHP.
- 评估了气道炎症,高反应性,氧化应激,Th2免疫反应和特定的分子通路 (TRPA1,p38 MAPK).
主要成果:
- 单单PS-MP对气道炎症和高反应性有轻微影响.
- 同时暴露于PS-MP和DEHP显著恶化了喘损伤.
- 联合暴露增加了氧化应激,Th2免疫反应,并激活了TRPA1和p38 MAPK通路.
- 抑制TRPA1或p38 MAPK通路可以减少喘症状的恶化.
结论:
- 同时暴露于PS-MP和DEHP会加剧过敏性喘.
- 这种恶化是由增加的氧化应激和炎症介导的.
- TRPA1-p38 MAPK通路在联合不良影响中发挥着关键作用.
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