中國醫藥大學機構典藏 China Medical University Repository, Taiwan:Item 310903500/6262
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    jsp.display-item.identifier=請使用永久網址來引用或連結此文件: http://ir.cmu.edu.tw/ir/handle/310903500/6262


    题名: ROS Mediates Baicalin-induced Apoptosis in Human ROS Mediates Baicalin-induced Apoptosis in Human Promyelocytic Leukemia HL-60 Cells through the Expression of the Gadd153 and Mitochondrial-dependent Pathway
    作者: (Lu H. F.)、(Hsueh S. C.)、(Ho Y. T.,)、高銘欽(Ming-Ching Kao)、楊家欣、(Chiu T. T.,)、(Huang S. Y.,)、(Lin C. C.)、鍾景光(Jing-Gung Chung)*
    贡献者: 生命科學院生物科技學系;中國附醫醫學研究部
    关键词: Baicalin;apoptosis;ROS;Gadd153;mitochondria;HL-60
    日期: 2007.01
    上传时间: 2009-08-25 14:39:33 (UTC+8)
    摘要: Background: Chemotherapy agents, particularly those that can induce apoptosis, are the major intervening strategy in the treatment of leukemia. In this study, we investigated the effects of baicalin (a compound obtained from Scutellaria baicalensis Georgi and S. rivularis Benth Labiateae) on the viability, induction of apoptosis and associated mechanism in human leukemia HL-60 cells. Materials and Methods: The cell viability and apoptosis was examined by flow cytometric analysis. The results showed that baicalin induced cytotoxicity in a dose- and time-dependent manner through the activation of caspase-3, as shown by treatment of HL-60 cells with an inhibitor of caspase-3 (z-VAD-fmk). Baicalin increased the levels of ROS, Ca2+ and decreased mitochondrial membrane potential in HL-60 cells. Western blot demonstrated that baicalin promoted the levels of Gadd153, Bax, cytochrome c and caspase-3 and -12, but decreased the levels of Grp78 and Bcl-2 in HL-60 cells. Conclusion: Baicalin was found to induce apoptosis in HL-60 cells through multiple pathways.
    關聯: ANTICANCER RESEARCH 27(1A ):117 ~126
    显示于类别:[生物科技學系暨碩士班] 期刊論文

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