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聚乙烯纳米塑料的暴露导致心肌细胞上的铁亡

Huifang Niu¹, Wen Li²

¹School of Pharmacy, Xinxiang Medical University, 453003, Xinxiang, Henan, China; School of Public Health, Xinxiang Medical University, 453003, Xinxiang, Henan, China.

Environmental pollution (Barking, Essex : 1987)

|June 18, 2025

概括

纳米塑料通过增加铁和氧化应激,诱导心脏细胞中的铁亡. 这种由纳米塑料驱动的细胞死亡机制凸显了与这些微小颗粒相关的心血管风险.

科学领域:

心血管生物学心血管生物学
毒理学毒理学毒理学
纳米医学是一种纳米医学.

背景情况:

纳米塑料可以进入心血管组织,通过反应性氧物种 (ROS) 可能造成伤害.
纳米塑料在铁相关疾病 (如铁亡) 中的作用尚不清楚.

研究的目的:

为了研究100nm聚烯纳米粒子 (PS-NP) 对大鼠心肌细胞的影响.
确定PS-NPs是否会诱导心肌细胞中的铁亡,并阐明底层机制.

主要方法:

主要的老鼠心肌细胞被暴露在PS-NP中.
评估了线粒体ROS,膜潜力,铁积累和脂质过氧化.
分析了细胞活力和与铁死相关的蛋白质的表达 (COX2,ACSL4,GPX4).
研究了除胺 (DFO) 对PS-NP诱导毒性的影响.
检查了自和NF-κB-IL6信号通路的激活.

主要成果:

PS-NP被心肌细胞内化,增加线粒体ROS和铁水平.
PS-NPs诱导了脂质过氧化,降低了线粒体膜潜能,并降低了细胞活力.
观察到对亲铁素蛋白 (COX2,ACSL4) 的上调和GPX4的下调.
通过降低铁和脂质过氧化,deferoxamine (DFO) 治疗挽救了细胞活力.
在PS-NP暴露后,自和NF-κB-IL6通路被激活.

结论:

100nmPS-NP诱导心肌细胞中的铁亡.
通过增加铁的积累,氧化应激和脂质过氧化,PS-NPs会触发铁.
激活的自和NF-κB-IL6信号通路参与了细胞对PS-NPs的反应.

关键词:

自自是一种自的过程.铁性化 (ferroptosis) 是一种炎症因子是炎症因子的一个因素.聚乙烯纳米塑料的聚乙烯纳米塑料.

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