悖论:黄素是一种天然抗氧化剂,通过过度反应性氧气物种抑制骨髓瘤细胞
Chunfeng Xu1, Mingjie Wang1, Behrouz Zandieh Doulabi1
1Department of Oral Cell Biology, Academic Centre for Dentistry Amsterdam (ACTA), Vrije Universiteit Amsterdam and University of Amsterdam, 1081 LA Amsterdam, The Netherlands.
International journal of molecular sciences
|August 12, 2023
概括
黄素 (CUR) 显示出治疗骨髓瘤 (OS) 和帮助骨修复的潜力. 令人惊的是,CUR增加了OS细胞中有害的活性氧物种 (ROS),导致亡,尽管增强了抗氧化防御.
科学领域:
- 生物医学工程 生物医学工程
- 在瘤学瘤学.
- 生物化学 生物化学
背景情况:
- 骨髓瘤 (OS) 是一种侵袭性骨癌,通常需要进行广泛的手术,导致关键骨缺陷和降低生活质量.
- 一种理想的OS治疗方法应该既具有抗癌性质,又能促进骨再生.
- 黄素 (CUR) 在OS治疗和骨再生方面表现有前途,但其在OS抑制中的机制尚未完全理解.
研究的目的:
- 研究黄素 (CUR) 抑制骨髓瘤 (OS) 发展的机制.
- 探索反应性氧物种 (ROS) 和核因素红色素2 (NRF2) 途径在CUR对OS细胞的影响中的作用.
主要方法:
- 在体外研究使用MG-63骨髓瘤细胞治疗不同度的黄素 (CUR) (10和20微米).
- 评估细胞内ROS水平,DNA损伤和亡.
- 分析NRF2蛋白水平和NRF2调节的抗氧化酶基因的表达.
主要成果:
- 黄素 (CUR) 治疗 (10和20微米) 在MG-63细胞中显著增加了细胞内ROS水平.
- 在骨髓瘤细胞中,CUR诱导了DNA损伤和随后的亡.
- 尽管ROS增加,但CUR也提高了NRF2蛋白水平,并上调了NRF2依赖抗氧化酶基因表达.
结论:
- 黄素 (CUR) 通过诱导氧化应激和亡,对骨髓瘤 (OS) 产生抗癌作用.
- 该研究揭示了一个复杂的相互作用,其中CUR增加ROS和DNA损伤,导致OS细胞死亡,即使在激活NRF2介导的抗氧化反应时也是如此.
- 这些发现为CUR对骨髓瘤的治疗潜力提供了新的见解,表明涉及氧化应激诱导的双重机制.
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