多基因学揭示非细胞化微塑料诱导结肠炎症损伤通过胆汁酸-肠道微生物群相互作用和屏障功能障碍
Junjie Chen1, Yixian Cheng1, Rui Fu1
1Department of General Surgery, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230022, China.
ACS applied materials & interfaces
|July 19, 2025
概括
非细胞化微塑料 (MPs) 通过破坏肠肝轴和胆酸代谢,引起结肠炎症和损伤. 这项研究揭示了微塑料毒性的新途径.
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:
- 微塑料 (MPs) 是全球污染物,对肠道毒性存在新的担忧.
- 非细胞化MPs (NPMs) 引起结肠炎症,但其机制尚未完全理解.
研究的目的:
- 在小鼠模型中研究10微米聚烯MP (PS MP) 诱导结肠炎症和损伤的机制.
- 阐明肠肝轴和胆酸代谢在NPM诱导的毒性中的作用.
主要方法:
- 建立一个BALB/c小鼠模型,长期口服暴露于10微米PS MPs.
- 评估结肠的氧化还原平衡,免疫平衡 (Th17/Treg比率,细胞因子) 和肠道屏障功能 (肌,紧密结节).
- 多组学分析以探索肝功能,肠道微生物群和胆酸 (BA) 代谢;在体外和体内验证特定的BA效应.
主要成果:
- PS MPs的暴露破坏了结肠的氧化还原平衡,诱导了氧化应激,并改变了免疫平衡.
- 肠道屏障功能受到损害,粘素和紧结蛋白表达减少.
- PS MPs通过肝肠轴失调了胆汁酸代谢,导致结肠胆汁酸的增加,特别是像TCDCA这样的结合BA,诱导了结肠上皮细胞亡.
结论:
- 非细胞化微塑料通过氧化应激,免疫失调和屏障功能障碍诱导结肠炎症和损伤.
- 微塑料的毒性通过一种新的"肝-BA-肠轴",涉及失调的胆酸代谢.
- 这项研究提供了对微塑料肠道毒性的跨器官机制的关键见解.
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