聚乙烯微纳米塑料的毒性和吸收在健康和克罗恩病的人类十二指肠芯片模型中
Davood Kharaghani1, Glen M DeLoid1, Ping He2
1Nanoscience and Advanced Materials Center, Environmental and Occupational Health Sciences Institute (EOHSI) and School of Public Health, Rutgers University, Piscataway, NJ 08854, USA.
Journal of hazardous materials
|March 1, 2025
概括
微型和纳米塑料 (MNP) 通过被动和活性机制被人类肠道吸收. 这项研究使用了肠上芯片模型来调查MNP吸收和毒性,发现伤害最小但潜在的免疫功能受损.
科学领域:
- 环境科学 环境科学
- 毒理学 毒理学 毒理学
- 胃肠病学 胃肠病学
背景情况:
- 微型和纳米塑料 (MNP) 是普遍存在的环境污染物,其肠道吸收机制尚不清楚.
- 之前的研究在简化模型中表明了MNP的被动和主动吸收途径.
研究的目的:
- 在人类肠上芯片 (IOC) 模型中研究25纳米聚乙烯贝金芯标记物MNP (AuPS25) 的毒性和吸收机制.
- 通过使用更具生理相关性的模型来验证先前的发现,其中包括初级人类肠道有机体.
主要方法:
- 开发一种微流体IOC模型,使用来自健康和克罗恩病的捐赠者的初级人肠上皮器官.
- 国际奥委会模型对AuPS25的暴露和毒性评估.
- RNA测序 (RNAseq) 分析以识别基因表达变化.
- 抑制剂研究以阐明吸收机制.
主要成果:
- 在健康和克罗恩氏病IOC模型中,AuPS25在24小时暴露后表现出最小的毒性.
- RNAseq发现了9个失调的基因,特别是干扰素α诱导蛋白6 (IFI6) 的下调.
- AuPS25的吸收通过被动扩散和活跃的,依赖于actin和dynamin的机制发生.
结论:
- 人体肠芯片模型证实,微和纳米塑料的吸收涉及被动和活性细胞过程.
- IFI6的下调表明先天免疫功能可能受到损害,这需要进一步调查健康后果.
- 这些发现支持先进的体外模型的实用性,用于研究MNP-肠道相互作用.
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