§ 瀏覽學位論文書目資料
  
系統識別號 U0002-2606201120054900
DOI 10.6846/TKU.2011.00934
論文名稱(中文) 人類卵巢癌細胞中 Chk2 蛋白的活化有助於黃芩素所誘導之 G2/M 細胞週期停滯
論文名稱(英文) Activation of Chk2 contributes to baicalein-induced G2/M cell cycle arrest in human ovarian cancer cells
第三語言論文名稱
校院名稱 淡江大學
系所名稱(中文) 化學學系碩士班
系所名稱(英文) Department of Chemistry
外國學位學校名稱
外國學位學院名稱
外國學位研究所名稱
學年度 99
學期 2
出版年 100
研究生(中文) 邵韋勳
研究生(英文) Wei-Syun Shao
學號 698160180
學位類別 碩士
語言別 繁體中文
第二語言別
口試日期 2011-06-16
論文頁數 53頁
口試委員 指導教授 - 莊子超
委員 - 陳銘凱
委員 - 許世忠
關鍵字(中) 細胞檢查點激酶
細胞週期
黃芩素
關鍵字(英) Chk2
G2/M arrest
Baicalein
第三語言關鍵字
學科別分類
中文摘要
類黃酮化合物是一種天然多酚類化合物,其持續攝取已經是被證實是可以促進身體健康、預防疾病產生以及防止癌症生成。在本研究中我們評估了類黃酮化合物-黃芩素 (Baicalein) 在人類卵巢癌的抗癌效果。經由實驗結果發現,在黃芩素的作用下,無論是隨著藥物作用濃度的提升或者是隨著作用時間的拉長,都會使得人類卵巢癌細胞之細胞生長能力受到明顯的抑制。然而,這些卵巢癌細胞在黃芩素作用下所導致的細胞生長抑制效果,是透過細胞週期 G2/M 停滯所造成。另外,經由實驗結果發現,黃芩素能夠誘導卵巢癌細胞內活性氧化物質 (ROS) 的生成量增加、H2AX 蛋白磷酸化和 Chk2蛋白的活化。除此之外,一些細胞週期 G2/M 的調控蛋白,如:Cdc25C、 Cdk1 以及 cyclin B1之蛋白質表現量也會在黃芩素的作用下而明顯下滑。綜合以上結果,人類卵巢癌細胞在黃芩素作用下所造成的細胞週期 G2/M 停滯現象,可能是由於 ROS 所導致的 DNA 受損而引發。
英文摘要
Baicalein has been reported to exhibit anti-tumor activities. In this study, we examined the anti-proliferating effects of baicalein on ovarian cancer cells. We found that baicalein inhibited the cell growth of ovarian cancer cells. Besides, our results demonstrate that baicalein caused reactive oxygen species (ROS) generation, H2AX phosphorylation and Chk2 activation in ovarian cancer cells. Furthermore, we also observed that G2/M regulatory molecules such as Cdc25C, Cdk1, cyclin B1 were down-regulation by baicalein. Taken together, these data suggest baicalein may generate ROS to cause DNA damage and then results in G2/M arrest in ovarian cancer cells.
第三語言摘要
論文目次
第一章 緒論...1
第一節 細胞檢查點激酶2...1
第二節 黃芩素...10
第二章 實驗目的...23
第三章 材料與方法...24
第四章 結果...28
第一節 實驗結果...28
第二節 實驗圖表...33
第五章 討論...39
第六章 結論...43
第七章 參考文獻...44
附錄一...53
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