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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/16458

    Title: Chrysophanol induces necrosis through the production of ROS and alteration of ATP levels in J5 human liver cancer cells
    Authors: 呂啟誠;Lu, Chi-Cheng;楊家欣;Yang, Jai-Sing;黃安正;Huang, An-Cheng;夏德椿;Hsia, Te-Chun;周淑姿;Chou, Su-Tze;郭昭麟;Kuo, Chao-Lin;呂旭峰;Lu, Hsu-Feng;李宗翰;Lee, Tsung-Han;Wellington, G.Wood;鍾景光;Chung, Jing-Gung
    Contributors: 生物科技學系
    Keywords: "Adenosine triphosphate;Chrysophanol;J5 human liver cancer cells;Necrosis;Reactive oxygen species;"
    Date: 2010-07
    Issue Date: 2012-11-23 17:13:22 (UTC+8)
    Abstract: "Anthraquinone compounds have been shown to induce apoptosis in different cancer cell
    types. Effects of chrysophanol, an anthraquinone compound, on cancer cell death have not
    been well studied. The goal of this study was to examine if chrysophanol had cytotoxic effects
    and if such effects involved apoptosis or necrosis in J5 human liver cancer cells. Chrysophanol induced necrosis in J5 cells in a dose- and time-dependent manner. Non-apoptotic cell
    death was induced by chrysophanol in J5 cells and was characterized by caspase independence, delayed externalization of phosphatidylserine and plasma membrane disruption.
    Blockage of apoptotic induction by a general caspase inhibitor (z-VAD-fmk) failed to protect
    cells against chrysophanol-induced cell death. The levels of reactive oxygen species production and loss of mitochondrial membrane potential (DCm) were also determined to assess the
    effects of chrysophanol. However, reductions in adenosine triphosphate levels and increases
    in lactate dehydrogenase activity indicated that chrysophanol stimulated necrotic cell death.
    In summary, human liver cancer cells treated with chrysophanol exhibited a cellular pattern
    associated with necrosis and not apoptosis."
    Appears in Collections:[生物科技學系] 期刊論文

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