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氧化铜纳米颗粒通过触发细胞亡诱导肺炎

Xiaojing Zhang¹, Zhongqi Peng¹, Qian Wang¹

¹Department of hygienic toxicology and pathology, West China School of Public Health and West China Fourth Hospital, Sichuan University, Chengdu 610041, China.

|April 3, 2025

概括

氧化铜纳米颗粒 (CuO NPs) 通过诱导一种称为cuproptosis的过程,在小鼠中引起肺炎. 这涉及细胞内铜的增加和特定蛋白质的激活,导致呼吸系统毒性.

科学领域:

环境毒理学环境毒理学
纳米材料的安全性
细胞生物学细胞生物学

背景情况:

氧化铜纳米粒子 (CuO NPs) 在工业上得到广泛应用.
对CuO NP的毒性存在担忧,特别是对肺部的影响.
CuO NP诱导的肺炎的确切机制尚不清楚.

研究的目的:

调查CuO NP诱导的肺炎及其潜在机制.
为了探索细胞亡在CuO NP毒性的作用.
为了阐明涉及的特定分子通路.

主要方法:

对C57BL/6小鼠和MH-S细胞通过内灌注暴露于CuONP.
肺组织的组织病理学检查.
测量细胞内铜度和铜症标志物 (FDX1,DLST,DLAT,CTR1) 的测量.
转录序列和代谢学分析.
与FDX1表达的干扰.

主要成果:

在小鼠中,CuO NPs诱导了显著的肺炎.
在肺组织和细胞中,细胞内Cu2+水平和cuproptosis指标升高.
转录和代谢学数据证实了CuO NP诱导的和炎症.
在CuO NP诱导的cuproptosis期间,中白素-17A (IL-17A) 水平增加.
FDX1干扰减轻了cuproptosis和IL-17A的释放.

结论:

CuO NPs通过FDX1-介导的cuproptosis引发肺炎.
细胞内铜积累和cuproptosis通路的激活是关键机制.
这项研究揭示了CuO NP呼吸道毒性的cuproptosis驱动的新途径.

关键词:

铜氧化物纳米粒子铜氧化物纳米粒子这种疾病叫做cuproptosis.铁素是一种铁素.互乐金17a是一种肺炎是一种肺炎.

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