Nrf2激活减轻肝细胞中的银纳米颗粒诱导的铁
Ruirui Wang1, Jiaqi Lan1, Xinyue Wang1
1Department of Clinical Laboratory, The First Affiliated Hospital of Bengbu Medical University, Bengbu, Anhui 233030, China.
Chemical research in toxicology
|September 1, 2025
概括
银纳米粒子 (AgNPs) 在肝细胞中诱导铁. 通过稳定Nrf2,减少氧化应激和调节铁含量,Nrf2通路对此进行保护.
科学领域:
- 纳米技术
- 毒理学
- 细胞生物学
背景情况:
- 银纳米粒子 (AgNP) 在消费品中广泛使用.
- 存在关于AgNP毒性的担忧,特别是肝脏积累和氧化应激.
- AgNP诱导的肝毒性的分子机制尚未完全理解.
研究的目的:
- 在肝细胞中研究AgNP毒性的分子机制.
- 确定AgNP是否会诱导肝细胞中的铁.
- 阐明Nrf2信号在AgNP诱导的铁死中的作用.
主要方法:
- 对小鼠肝细胞和HepG2细胞的AgNP暴露.
- 转录组分析以确定细胞反应.
- 西方涂抹和基因表达分析以研究蛋白质和基因调节.
主要成果:
- 在肝细胞和HepG2细胞中引发铁.
- 转录组分析显示铁死是对AgNPs的主要反应.
- 通过p62/Keap1相互作用的Nrf2激活,可以防止AgNP诱导的铁.
- Nrf2调节的抗氧化酶 (NQO1,HO-1) 和铁储蛋白 (FTH,FTL) 的表达.
结论:
- 通过涉及氧化应激和铁失调的机制,AgNP诱导肝细胞中的铁.
- Nrf2信号对AgNP诱导的铁起着关键的保护作用.
- 了解这些途径对于评估AgNP安全性和开发干预措施至关重要.
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