摘要
活性氧(reactive oxygen specis ROS)在三氧化二砷(arsenic trioxide,As_2O_3)诱导肿瘤细胞凋亡中扮演重要角色。本研究用一种天然蒽醌类物质——大黄素(emodin)作为提高HeLa细胞ROS水平的手段,考察其对As_2O_3促凋亡敏感性的影响,并探究可能涉及的信号传导机制。结果显示大黄素10μmol/L提高ROS并增加了HeLa细胞在As_2O_32μmol/L作用下的凋亡率,对正常成纤维细胞却无影响。该联合作用可以促进HeLa细胞线粒体跨膜电位降低;抑制转录因子NF-kB激活。本研究提示:大黄素通过提高ROS介导凋亡信号传导的增强和生存信号传导的抑制,增加HeLa细胞对As_2O_3促凋亡的敏感性。
Since reactive oxygen species(ROS) has been known to play an important role in apop-tosis induced by arsenic trioxide,we attempt to elevate the cellular ROS level on HeLa cell by an natural anthraquinone-emodin.then to study its effect on apoptotic sensitivity to arsenic,and finally to investigate the mechanisms of the involved signaling pathway. The results showed that emodin 10 micro-mol/L could enhance arsenic induced apoptosis via generation of ROS, whereas rendered no detectable effect on normal fibroblast. Increased ROS promoted mitochondrial transmembrane potential collapse; inhibited the activation of transcription factors NF-kappa B. The study elucidated that emodin sensitize HeLa cells via generation of ROS which result in enhancement of apoptosis signaling pathway and inhibition of survival signaling pathway.
出处
《实验生物学报》
CSCD
北大核心
2003年第6期465-475,共11页
Acta Biologiae Experimentalis Sinica
基金
国家自然科学基金(30170475)