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细颗粒物 (PM2.5) 通过诱导Caco-2细胞中的氧化应激和PI3K/AKT介导的炎症来破坏肠道屏障功能

Ruiwei Liao¹, Qianwen Zhang¹, Yao Lu¹

¹School of Basic Medical Sciences, Guangzhou University of Chinese Medicine, China No. 232, East Waihuan Road, Guangzhou Higher Education Mega Centre, Guangzhou 510006, China.

International journal of molecular sciences

|September 13, 2025

概括

暴露于细颗粒物 (PM2.5) 损害了肠道屏障,增加了透性和炎症. 这通过PI3K/AKT信号传递,反应性氧物种生成和降低β-catenin发生,导致胃肠道问题.

科学领域:

环境健康环境健康
胃肠病学胃肠病学
细胞生物学细胞生物学

背景情况:

细颗粒物 (PM2.5) 与胃肠道疾病有关,但其对肠道功能的确切影响尚不清楚.
了解PM2.5的影响对公共卫生至关重要,特别是关于环境暴露和肠道健康.

研究的目的:

通过环境暴露细胞模型,研究PM2.5改变肠道屏障功能的机制.
为了确定参与PM2.5诱导的肠道透性的关键分子通路.

主要方法:

一个体外细胞模型 (Caco-2细胞) 暴露于PM2.5.5.
使用跨上皮电阻 (TEER) 和FITC-dextran测试来评估肠道透性.
测量了紧结蛋白β-catenin,炎症性细胞因子 (TNF-α,IL-6),PI3K/AKT通路组件以及氧化应激标志物 (ROS,马隆迪甲) 的表达.

主要成果:

暴露于PM2.5显著增加了肠道透性,由降低TEER和增加FITC-dextran透率证明.
暴露在PM2.5下调β-catenin表达和CTNNB1基因水平,破坏细胞间连接.
在暴露于PM2.5的细胞中观察到炎症性细胞因子的升高,氧化应激增加 (ROS) 和PI3K/AKT通路的激活.
抑制PI3K/AKT和清理ROS减轻PM2.5诱导的肠壁功能障碍.

结论:

暴露于PM2.5会损害Caco-2细胞中的肠道屏障完整性.
PI3K/AKT信号通路和ROS生成是PM2.5诱导的肠道炎症和超透性的关键调解者.
针对这些途径可能为减轻PM2.5相关的胃肠道损伤提供治疗策略.

关键词:

通过PI3K/AKT路径.对于PM2.5来说,这是一个很好的例子.这是一种炎症炎症炎症炎症.肠道的通透性肠道的通透性氧化应激是一种氧化应激.

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