GL-V9通过MAPK信号通路诱导CML细胞的亡
Fengyu Jiang1, Yangyang Xue1, Qin Zhang1
1Jiangsu Collaborative Innovation Center of Chinese Medicinal Resources Industrialization, School of Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, PR China.
Heliyon
|August 5, 2024
概括
GL-V9是一种沃贡因衍生物,有效降低慢性髓性白血病 (CML) 细胞活力,并诱导细胞亡. 这种化合物通过影响线粒体功能和激活MAPK通路,显示出作为CML新型治疗剂的潜力.
科学领域:
- 生物化学 生物化学
- 分子生物学分子生物学
- 在瘤学瘤学.
背景情况:
- 沃戈宁衍生物在各种癌症中表现出抗瘤特性.
- 在慢性髓性白血病 (CML) 中GL-V9的治疗潜力以前没有被研究过.
研究的目的:
- 为了评估GL-V9对CML细胞的疗效.
- 阐明GL-V9在CML中的作用的基本机制.
主要方法:
- 细胞活力测定试验
- 附件V/PI染色用于检测亡.
- JC-1测定用于测量线粒体膜潜力的评估.
- 反应性氧物种 (ROS) 测量测量
- 转录基因测序的测序
- 西方斑点分析分析
主要成果:
- GL-V9显著降低了CML细胞活力,以剂量依赖的方式.
- GL-V9诱导了亡和线粒体膜潜能 (ΔΨm) 的降低.
- GL-V9调节了活性氧物种 (ROS) 水平,并激活了MAPK通路.
结论:
- GL-V9对CML细胞表现出显著的抗白血病作用.
- 该机制涉及亡诱导,线粒体功能障碍和MAPK通路激活.
- GL-V9代表了慢性髓性白血病的一个有前途的治疗候选者.
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