聚烯微塑料通过激活大脑TLR4破坏肠-大脑轴,并通过TLR4/MyD88/NF-κB通路损害海马突触
1College of Food Science and Engineering, Jilin University, Changchun 130062, China.
Journal of agricultural and food chemistry
|February 25, 2026
概括
较小的聚烯微塑料 (PS-MPs) 可以损害肠道和大脑,导致神经炎症和突触损伤. 亚微米PS-MPs存在神经退行症的风险,需要进一步研究慢性暴露的影响.
科学领域:
- 环境科学 环境科学
- 毒理学 毒理学 毒理学
- 神经科学是一个神经科学.
背景情况:
- 聚烯微塑料 (PS-MPs) 在全球普遍存在.
- 对于PS-MP神经毒性的机制尚不清楚.
研究的目的:
- 调查PS-MP诱导的肠道和中枢神经系统 (CNS) 的损伤.
- 阐明PS-MP神经毒性的潜在机制.
主要方法:
- 评估了PS-MPs的大小依赖的生物积累和屏障透.
- 分析了肠道失调,脂多糖 (LPS) 转移和血脑屏障 (BBB) 完整性.
- 检查了托尔类受体4 (TLR4) /MyD88/NF-κB信号通路和促炎性细胞因子水平.
- 在海马体中评估了突触损伤.
主要成果:
- PS-MPs显示了尺寸依赖的生物积累和屏障透,较小的颗粒 (≤1μm) 透更有效.
- 1微米PS-MPs诱导最大的神经炎症,尽管与500纳米颗粒相比,生物分布较低.
- PS-MPs引起肠道失调,导致循环LPS增加和BBB妥协.
- 观察到TLR4/MyD88/NF-κB通路的激活和高水平的促炎细胞因子,导致海马突触损伤.
结论:
- 较小的PS-MP (≤1μm) 作为神经退行症的潜在危险因素.
- 肠道失调和LPS在受损的BBB中的转移是关键机制.
- 迫切需要对慢性PS-MP暴露的影响进行评估.
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