Evodiamine,a constituent of Evodiae Fructus,induces anti-proliferating effects in tumor cells |
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| Authors: | Fei Xiao Fang Wang Ben Xiang Li Tei Jin Tashiro Shin-ichi Minami Mutsuhiko Xing De Jun Ikejima Takashi |
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| Institution: | College of Life Sciences, Jilin University, Changchun 130012, China;Jilin Institute of Natural Medicine, Changchun 130012, China;United Research Center for Intelligent Materials, Department of Chemistry, Jilin University, Changchun 130021, China;Department of Clinical and Biomedical Sciences, Showa College of Pharmaceutical Sciences, Tokyo 194–8543;Department of Parasitology, Yokohama City University School of Medicine, 3–5 Fukuura, Kanazawa-ku, Yokohama 236–0004;Jilin Provincial Cancer Center Hospital, Jilin, 130012, China;China-Japan Research Institute of Medical and Pharmaceutical Sciences, Shenyang Pharmaceutical University, Shenyang,103 Wenhua Road, Liaoning Province, 110016, China |
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| Abstract: | We found that evodiamine, a major alkaloidal component of Evodiae Fructus (Goshuyu in Japan), inhibited proliferation of several tumor cell lines, but had less effect on human peripheral blood mononuclear cells (PBMC). We used human cervical cancer cells, HeLa, as a model to elucidate the molecular mechanisms of evodiamine-induced tumor cell death. The results showed that evodiamine induced oligonucleosomal fragmentation of DNA in HeLa cells and increased the activity of caspase-3, but not that of caspase-1, in vitro . Both evodiamine-induced DNA fragmentation and caspase-3 activity were effectively inhibited by a caspase-3 inhibitor, z-DEVD-fmk (z-Asp-Glu-Val-Asp-fmk). In addition, evodiamine increased the expression of the apoptosis inducer Bax, but decreased the expression of the apoptosis suppressor Bcl-2 in mitochondria. Taken together, our data indicated that evodiamine alters the balance of Bcl-2 and Bax gene expression and induces apoptosis through the caspase pathway in HeLa cells. (Cancer Sci 2003; 94: 92–98) |
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