在氧化压力转变为还原压力的过程中,线核动力学会增强人体氨酸细胞中素诱导的恶性转化潜力
Qianlei Yang1, Xingrun Li1, Qi Kong2
1Department of Toxicology, School of Public Health, Jiangsu Key Laboratory of Preventive and Translational Medicine for Major Chronic Non-communicable Diseases, MOE Key Laboratory of Geriatric Diseases and Immunology, Suzhou Medical College of Soochow University, Suzhou, Jiangsu 215123, China.
Journal of hazardous materials
|February 7, 2026
概括
暴露将细胞从氧化压力转移到还原压力,引发恶性转变. 这一过程涉及核因子红色素-2相关因子2 (NRF2) 和粒,提供了新的治疗点.
科学领域:
- 细胞生物学 细胞生物学
- 毒理学 毒理学 毒理学
- 癌症研究 癌症研究
背景情况:
- 氧化应激在引起的致癌性中的作用已经确立,但过渡到还原性应激和随后的恶性转变仍然不太清楚.
- 了解驱动在氧化还原应激下恶性转变的细胞机制,对于开发有效的干预措施至关重要.
研究的目的:
- 研究由低剂量酸 (NaAsO2) 诱导的人类角质细胞中由氧化应激转化为还原应激的氧化应激过渡.
- 阐明核因子红色素-2相关因子2 (NRF2) 和菌体在酸盐诱导的恶性转变中的作用.
主要方法:
- 长期,低剂量化 (NaAsO2) 暴露于不朽的人类角质细胞 (HaCaT细胞).
- 评估反应性氧物种 (ROS) 水平,还原性稳态和线粒体动态.
- 对PTEN诱导的PINK1 (PINK1) -PARK2 (Parkin) 依赖的线粒细胞衰变途径的研究.
- 利用NRF2siRNA和环素A (CsA) 来调节线粒.
主要成果:
- 长时间的NaAsO2暴露诱导了从氧化应激过渡到还原应激.
- 持续的NRF2激活促进了线粒,通过PINK1-Parkin通路从42.8%增加到96%.
- 抑制NRF2或线粒细胞衰变部分阻断了恶性转变过程.
结论:
- NRF2在动态调节氧化还原稳态中发挥着至关重要的作用.
- 线性是酸盐诱导的细胞恶性转变中的一个中心机制.
- 向线粒菌为预防和治疗引起的癌症提供了潜在的策略.
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