[Emodin sensitizes HeLa cell to arsenic trioxide induced apoptosis via the reactive oxygen species-mediated signaling pathways].
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.
Yang
Jie
J
Department of Cell Biology, Shanghai Second Medical University, Shanghai 200025, China.
Tang
Xue Ming
XM
Li
Hui
H
Shi
Gui Ying
GY
Zhu
Ping
P
Jin
Hui Fang
HF
Yi
Jing
J
D017209:Apoptosis / Q000187:drug effects*; D000077237:Arsenic Trioxide; D001152:Arsenicals / Q000494:pharmacology*; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D002648:Child; D004357:Drug Synergism; D004642:Emodin / Q000494:pharmacology*; D005347:Fibroblasts / Q000166:cytology; D006367:HeLa Cells; D006801:Humans; D008564:Membrane Potentials / Q000187:drug effects; D008928:Mitochondria / Q000502:physiology; D016328:NF-kappa B / Q000378:metabolism; D010087:Oxides / Q000494:pharmacology*; D017382:Reactive Oxygen Species / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects*; D020298:U937 Cells
D001152:Arsenicals; D016328:NF-kappa B; D010087:Oxides; D017382:Reactive Oxygen Species; D004642:Emodin; D000077237:Arsenic Trioxide