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    CMUR > General Education Center > Research papers >  Item 310903500/12218
    Please use this identifier to cite or link to this item: http://ir.cmu.edu.tw/ir/handle/310903500/12218


    Title: 熊果酸及齊墩果酸誘導人類肺癌細胞凋亡
    Ursolic Acid and Oleanolic Acid Induced Apoptosis in Human Lung Cancer Cells
    Authors: 黃雯雯(Huang,Wen-Wen)
    Contributors: 通識教育中心
    Keywords: 熊果酸;齊墩果酸;人類肺癌細胞株;細胞凋亡;ursolic acid;oleanolic acid;human lung cancer cell lines;apoptosis
    Date: 2005-07-31
    Issue Date: 2009-09-01 15:47:35 (UTC+8)
    Abstract: 熊果酸(ursolic acid)及齊墩果酸(oleanolic acid)皆屬pentacyclic triterpene化合物,有研究顯示此類化合物具細胞毒殺作用(cytotoxicity),可誘導細胞分化(differentiation),並有抗突變(antimutagenic)作用及抗病毒(antiviral)等活性。我們研究發現ursolic acid對人類血癌細胞株(K562, U937),人類大細胞肺癌株(NCI-H460),人類肺癌鱗狀上皮細胞株(CH-27),人類肺癌細胞株(H1355)皆具抑制效果,其中對CH-27細胞株,NCI-H460細胞株,H1355細胞株,抑制效果更為顯著,IC50分別為50、100 and 300μg/ml;而oleanolic acid對上述細胞株的毒殺作用似乎並不明顯。為更進一步探討熊果酸(ursolic acid)之抗癌機制,因此我們以熊果酸處理CH27細胞,進行DNA電泳分析,發現有DNA裂解現象,至於細胞周期試驗顯示無論是熊果酸還是齊墩果酸對CH27細胞株的細胞周期無明顯滯留現象,顯示二者沒有抑制細胞周期的作用。經西方墨點法測試蛋白質,結果顯示Bcl-2蛋白質的量隨處理時間增長而增加,而Bax蛋白質量則有下降的趨勢,顯示其抑制癌細胞生長的作用可能是藉由細胞凋亡(apoptosis)的途徑產生,造成凋亡的原因可能是透過與Bcl-Xs蛋白質相關機制,同時Bax蛋白質量降低亦是熊果酸導致細胞凋亡的機轉之一,值得作更深入之探討。
    The compounds of pentacyclic triterpene (include ursolic acid and oleanolic acid) have been reported to raise anti-tumor activities. In this study, we investigated the anti-tumor effects of ursolic acid (UA) and oleanolic acid (OA) on human lung squamous cancer CH-27 cells, human lung large cell carcinoma NCI-H460 cells and human lung cancer H1355 cells lines. UA inhibited the cell proliferation with dose- and time- dependence, and the IC50 of UA on CH27, NCI-H460 and H1355 cells were 50, 100 and 300μg/ml, respectively. But OA seemed to have no cytotoxic effect on CH27, NCI-H460 and H1355 cells. UA showed to have better inhibitory effect on CH-27 than the other two (NCI-H460, H1355). We focused on the apoptosis experiment of CH-27 cells and found a phenomenon of DNA fragmentation. Our results were consistent with the published research data as evidenced by the up-regulation of pro-apoptotic Bax protein and the down-regulation of anti-apoptotic Bcl-2 protein during UA induced apoptosis. The precise mechanism of the induction of apoptosis by UA in CH27 cells will be the subject for further investigation in our research.
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