期刊
FREE RADICAL BIOLOGY AND MEDICINE
卷 40, 期 12, 页码 2183-2197出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2006.02.016
关键词
redox; apoptosis; NF-kappa B; free radical
We previously found that emodin produced reactive oxygen species (ROS) intracellularly, In various tumor cells at low doses it enhances the cytotoxicity of As2O3, and at higher doses it renders cytotoxicity independently in vitro and in vivo. The effects involve redox-mediated inhibition of NF-kappa B activation. In this study, we focus on the mechanisms by which emodin inhibits NF-kappa B activation. Results in HeLa cells demonstrated that emodin at high doses or in combination with As2O3, via generation of ROS especially in the nucleus, altered subcellular redox equilibrium and thus oxidized the redox-sensitive site on NF-kappa B and prevented its binding to the target DNA. In vivo study showed that tumors exposed to the arsenic/emodin cotreatment had dramatically smaller sizes and weaker antioxidant capacity, compared with arsenic alone. NF-kappa B binding and transactivation were inhibited in these tumors. These data help in the understanding of the mechanisms by which manipulation of cellular redox and NF-kappa B activation may enhance chemotherapy. (c) 2006 Elsevier Inc. All rights reserved.
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