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    Please use this identifier to cite or link to this item: http://ir.cnu.edu.tw/handle/310902800/4452

    標題: DBM及其衍生物引發人類直腸癌細胞凋亡機制的研究
    Studies on the induction of apoptosis in human colorectal carcinoma cells by dibenzoylmethane and its derivatives
    作者: 黃玫貞
    Mei-Chen Huang
    貢獻者: 林朝賢
    關鍵字: 細胞凋亡
    細胞色素 c
    cytochrome c
    日期: 2003
    上傳時間: 2008-10-08 15:45:39 (UTC+8)
    摘要: Dibenzoylmethane (DBM)為存在於甘草中之微量成分,研究顯示DBM具有抑制腫瘤生成的活性,但其他活性之研究並不多。Hydroxydibenzoylmethane(HDBM)及2-Hydroxy-5-
    methyldibenzoylmethane (HMDBM)為DBM衍生物,皆具有b-diketone及共軛雙鍵特色。本實驗首先比較DBM及其衍生物對於COLO 205細胞生長速率之影響,實驗結果發現DBM 及其衍生物皆可抑制COLO 205細胞生長,在caspase活性測試中亦發現DBM、HDBM及HMDBM可誘使細胞內各種caspase活性上升,而趨動下游訊息進一歩造成細胞內的DNA產生片段化現象,其中以HDBM引發細胞凋亡之能力為最強, HMDBM次之,而DBM最弱。因此,我們進一步探討HDBM引發細胞凋亡之分子機制,由西方墨點法實驗中顯示HDBM可誘使COLO 205細胞內的cyclin D3、P21及Bax蛋白表現增加,Bcl-XL蛋白質表現下降,而Bcl-2及Bad卻不受影響,同時HDBM亦藉由影響Bcl-XL與Bax的表現,而促使粒線體內的cytochrome c流失至細胞質中而造成caspase-9的活化,且促使caspase-9進而活化capsase-3。接著,活化的caspase-3
    更進一步造成PARP及DFF-45降解而使caspase-activated deoxyribonuclease能進入細胞核內,終至造成DNA的片段化。由以上實驗結果我們認為HDBM對於癌症的預防作用有所助益。
    DBM (dibenzoylmethane) is a minor constituent of licorice that has anti-
    mutagenic activity. However, its other biological activities are not well-
    know. The structurally related b-diketone, such as DBM, hydroxydibenzoylmethane
    (HDBM), hydroxymethyldibenzoylmethane (HMDBM), were able to induce apoptosis
    in colorectal carcinoma COLO 205 cells. Thus, the effect of structurally
    related b-diketone on cell viability, DNA fragmentation and caspase activity
    was assessed. The potency of these compounds on these features of apoptosis
    were in the order of :HDBM>HMDBM>DBM in colorectal carcinoma COLO 205
    cells. Here, we found that HDBM-induced apoptotic cell death was accompanied
    by upregulation of cyclin D3, Bax, and p21 and downregulation of Bcl-XL, while
    HDBM had no effect on the levels of Bcl-2 and Bad protein. These results
    indicate that HDBM allows caspase-activated deoxyribonuclease to enter nucleus
    and degrade chromosomal DNA and induces DFF-45 degradation. It is suggested
    that HDBM induced apoptosis is triggered by the release of cytochrome c into
    cytosol, procaspase-9 processing, activation of caspase-3 and caspase-2,
    degradation of PARP, and DNA fragmentation caused by the caspase-activated
    deoxyribonuclease through the digestion of DFF-45. The induction of apoptosis
    by HDBM may provide a pivotal mechanism for its cancer chemopreventive action.
    Appears in Collections:[生物科技系(所)] 博碩士論文

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