Yang Jie, Tang Xue Ming, Li Hui, Shi Gui Ying, Zhu Ping, Jin Hui Fang, Yi Jing
Department of Cell Biology, Shanghai Second Medical University, Shanghai 200025, China.
Shi Yan Sheng Wu Xue Bao. 2003 Dec;36(6):465-75.
Since reactive oxygen species(ROS) has been known to play an important role in apoptosis 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 micromol/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.
由于已知活性氧（ROS）在三氧化二砷诱导的细胞凋亡中起重要作用，我们尝试通过天然蒽醌——大黄素提高HeLa细胞中的细胞ROS水平，进而研究其对砷诱导凋亡敏感性的影响，最终探究相关信号通路的机制。结果显示，10微摩尔/升的大黄素可通过产生ROS增强砷诱导的细胞凋亡，而对正常成纤维细胞无明显影响。ROS增加促使线粒体跨膜电位崩溃；抑制转录因子NF-κB的激活。该研究阐明，大黄素通过产生ROS使HeLa细胞致敏，从而增强凋亡信号通路并抑制生存信号通路。
