中國醫藥大學機構典藏 China Medical University Repository, Taiwan:Item 310903500/50228
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    題名: 薑黃素奈米微粒引發順鉑抗藥性人類口腔癌細胞凋亡機制之研究
    Study of the Apoptotic Mechanisms Induced by Curcumin-loaded Nanoparticles in Cisplatin-resistant Human Oral Cancer Cells
    作者: 張佩穎;Pei-Ying Chang
    貢獻者: 牙醫學系碩士班
    關鍵詞: 順鉑抗藥性口腔癌細胞;水溶性薑黃素?;米微?;細胞凋亡;多重抗藥性蛋白質;活性氧分子;CAL27-cisplatin resistant human oral cancer cells (CAR cells);Curcumin nanoparticles (Cur-NPs);Apoptosis;Multiple drug resistance protein 1 (MDR1);Reactive oxygen species (ROS)
    日期: 2013-06-26
    上傳時間: 2013-10-02 10:56:34 (UTC+8)
    出版者: 中國醫藥大學
    摘要: 薑黃素是具有抗癌潛?的天然藥物，被證實能誘發多種癌細胞株死亡，但它對於順鉑抗藥性口腔癌細胞的效果目前仍未明。薑黃素的脂溶性特質，限制?它的生?使用?。本研究使用水溶性薑黃素?米微?，並探討它對於順鉑抗藥性口腔癌細胞（以下簡稱「細胞」）的效應與機轉。本研究結果發現薑黃素?米微?能引發細胞凋亡，但對正常的口腔牙齦纖維細胞與角化細胞則?具毒性。薑黃素?米微?在細胞內會誘發DNA 濃集與?解。與未經處?的細胞相較，經薑黃素?米微?處?過的細胞中能偵測到較高的Calcein-AM 濃?。薑黃素?米微?抑制多重抗藥性蛋白質（multiple drug resistance protein 1；MDR1）之蛋白質與mRNA 表現。經薑黃素?米微?處?的細胞，caspase-3 與caspase-9 的活性與表現?上升，而細胞凋亡現象則可藉由加入caspase 抑制劑（pan-caspase 的抑制劑z-VAD-fmk、caspase-3的抑制劑z-DEVD-fmk、caspase-9 的抑制劑z-LEHD-fmk）或抗氧化劑（N-acetylcysteine；NAC）?阻斷。經薑黃素?米微?處?的細胞，細胞內活性氧分子（reactive oxygen species；ROS）增加， cleaved caspase-3/caspase-9、cytochrome c、Apaf-1、AIF、Bax 的表現?提高，Bcl-2 則減少。我們的結果推?薑黃素?米微?是藉由抑制多重抗藥性蛋白質的表現，引發順鉑抗藥性口腔癌細胞內產生活性氧分子，而啟動細胞凋亡機轉，經由內在途徑引導細胞走向凋亡。有鑑於?床上已發現對順鉑具有抗藥性的口腔癌病?，水溶性薑黃素?米微??失為一個值得開發用以治?此?棘手案?的天然藥物。
    Curcumin is a polyphenolic compound which possesses anti-cancer potential. It has been shown to induce cell death in a variety of cancer cells, but its effect on CAL27-cisplatin-resistant human oral cancer cells (CAR cells) is still unknown. The poor bioavailability caused by low water solubility of curcumin has been highlighted as a major limiting factor. In this study, we utilized water-soluble PLGA curcumin nanoparticles (Cur-NPs), and investigated the effects of Cur-NPs on CAR cells. The results showed Cur-NPs induced apoptosis in CAR cells but exhibited low cytotoxicity to normal human gingival fibroblasts and
    human oral keratinocytes. Cur-NPs triggered DNA concentration, fragmentation and subsequent apoptosis. Compared to the untreated group, more detectable amount of calcein-AM accumulation was found in the treated CAR cells. Cur-NPs suppressed the protein and mRNA expression levels of multiple drug resistance protein 1 (MDR1). Both of
    the activity and the expression levels of caspases-3 and caspase-9 were elevated in the treated CAR cells. The Cur-NPs-triggered apoptosis was blocked by specific inhibitors of pan-caspase (z-VAD-fmk), caspase-3 (z-DEVD-fmk), caspase-9 (z-LEHD-fmk), as well as by antioxidant agent (N-acetylcysteine; NAC). Cur-NPs increased reactive oxygen species (ROS) production, up-regulated the protein expression levels of cleaved caspase-3/caspase-9, cytochrome c, Apaf-1, AIF, Bax and meanwhile down-regulated that of Bcl-2. Our results suggest that Cur-NPs triggered
    intrinsic apoptotic pathway through regulating the function of MDR1 and the production of ROS in CAR cells. Cur-NPs could be potentially efficacious in the treatment of cisplatin-resistant human oral cancer.
    顯示於類別:[牙醫學系暨碩博士班、口腔醫學產業碩士班] 博碩士論文

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