红氧调节的细胞响应机制与N-乙基尿素在人间介质干细胞中氧铁复合体的反应
A A Balakina1, V I Amozova2, T S Stupina2
1Federal Research Center of Problems of Chemical Physics and Medicinal Chemistry, Russian Academy of Sciences, Chernogolovka, Moscow Region, Russia. balakina@icp.ac.ru.
Bulletin of experimental biology and medicine
|March 28, 2025
概括
酸铁复合物与N-乙基尿素 (ETU) 通过增加自由基和一氧化,导致人类干细胞的细胞死亡. 它激活Nrf2/HO-1通路,同时抑制NF-κB,突出其细胞毒性作用中的氧化还原过程.
科学领域:
- 生物化学 生物化学
- 细胞生物学 细胞生物学
- 毒理学 毒理学 毒理学
背景情况:
- 酸铁复合物涉及到细胞的氧化还原过程.
- 了解它们对人类介质干细胞 (hMSCs) 的影响至关重要.
- 像Nrf2和NF-κB这样的氧敏感转录因子在细胞反应中起着关键作用.
研究的目的:
- 为了研究铁复合物与N-乙基尿素 (ETU) 对hMSCs的影响.
- 分析细胞死亡,自由基积累和转录因子活性 (Nrf2,NF-κB).
- 阐明氧化还原依赖机制在复合体细胞毒性中的作用.
主要方法:
- 在体外研究中使用人类介质干细胞模型.
- 细胞死亡和细胞内自由基水平的评估.
- 对Nrf2和NF-κB转录因子活动的分析.
主要成果:
- 该ETU综合体表现出显著的抗氧化和细胞毒性作用.
- 观察到一氧化物的细胞内积累增加.
- 在Nrf2/HO-1通路激活的同时,诱导了亡细胞死亡.
- 发生了由NF-κB介导的促炎性反应的抑制.
结论:
- 在hMSCs中,ETU酸铁复合物诱导了细胞亡和氧化应激.
- 红氧依赖的细胞过程对这个复杂的细胞毒性机制至关重要.
- 该研究强调了Nrf2和NF-κB通路在对ETU复合体的反应中的相互作用.
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