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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/86941

    Title: The crude extract of Corni Fructus induces apoptotic cell death through reactive oxygen species-modulated pathways in U-2 OS human osteosarcoma cells.
    Authors: Ching-Lung, L;Liao, Ching-Lung;Hsu, Shu-Chun;Hsu, Shu-Chun;Chien-Chih, Y;Yu, Chien-Chih;Yan, Jai-Sing;Yang, Jai-Sing;Tan, Nou-Ying;Tang, Nou-Ying;Wellington, G;Wood, Wellington Gibson;Jaung-Geng, L;Lin, Jaung-Geng;鍾景光*
    Contributors: 生物科技學系
    Keywords: U-2 OS human osteosarcoma cells;apoptosis;crude extract of Corni Fructus (CECF);reactive oxygen species (ROS)
    Date: 2014-09
    Issue Date: 2014-11-07 14:54:25 (UTC+8)
    Abstract: Crude extract of Corni Fructus (CECF) has been used in Traditional Chinese medicine for the treatment of different diseases for hundreds of years. The purpose of this study was to investigate the cytotoxic effects of CECF on U-2 OS human osteosarcoma cells. Flow cytometry was used for measuring the percentage of viable cells, cell-cycle distribution, apoptotic cells in sub-G1 phase, reactive oxygen species (ROS), Ca(2+) levels, and mitochondrial membrane potential (ΔΨm ). Comet assay and 4'-6-diamidino-2-phenylindole staining were used for examining DNA damage and condensation. Western blotting was used to examine apoptosis-associated protein levels in U-2 OS cells after exposed to CECF. Immunostaining and confocal laser system microscope were used to examine protein translocation after CECF incubation. CECF decreased the percentage of viability, induced DNA damage and DNA condensation, G₀/G₁ arrest, and apoptosis in U-2 OS cells. CECF-stimulated activities of caspase-8, caspase-9, and caspase-3, ROS, and Ca(2+) production, decreased ΔΨm levels of in U-2 OS cells. CECF increased protein levels of caspase-3, caspase-9, Bax, cytochrome c, GRP78, AIF, ATF-6α, Fas, TRAIL, p21, p27, and p16 which were associated with cell-cycle arrest and apoptosis. These findings suggest that CECF triggers apoptosis in U-2 OS cells via ROS-modulated caspase-dependent and -independent pathways.
    Copyright © 2012 Wiley Periodicals, Inc., a Wiley company.
    Relation: ENVIRONMENTAL TOXICOLOGY;29(9):1020-31.
    Appears in Collections:[生物科技學系] 期刊論文

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