中國醫藥大學機構典藏 China Medical University Repository, Taiwan:Item 310903500/24371
English  |  正體中文  |  简体中文  |  全文笔数/总笔数 : 29490/55136 (53%)
造访人次 : 1567669      在线人数 : 433
RC Version 7.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
搜寻范围 查询小技巧：
  • 您可在西文检索词汇前后加上"双引号"，以获取较精准的检索结果
  • 若欲以作者姓名搜寻，建议至进阶搜寻限定作者字段，可获得较完整数据
    •  进阶搜寻
    主页 ‧ 登入 ‧ 上传 ‧ 说明 ‧ 关于CMUR ‧ 管理 到手机版


    jsp.display-item.identifier=請使用永久網址來引用或連結此文件: http://ir.cmu.edu.tw/ir/handle/310903500/24371


    题名: 蘆薈大黃素誘導人類前骨髓白血病細胞株（HL-60）的細胞週期停止在G2/M期;Aloe-emodin induced in vitro G2/M phase arrest of cell cycle in human promyelocytic leukemia HL-60 cells
    作者: 陳宣嘉;Hsuan-Chia Chen
    贡献者: 中國醫藥學院醫學研究所
    关键词: 蘆薈大黃素;人類前骨髓白血病細胞株;細胞週期;Aloe-emodin;human promyelocytic leukemia HL-60 cells;cell cycle
    日期: 1992
    上传时间: 2009-12-23
    摘要: 在本篇研究中，藉由探討細胞增生（proliferation）、細胞週期（cell cycle）及細胞凋亡（apoptosis）等機制，評估蘆薈大黃素（aloe-emodin）對於人類前骨髓白血病細胞株（HL-60）抗癌的角色。由實驗數據發現，蘆薈大黃素對人類前骨髓白血病細胞株會抑制細胞增生、細胞週期停止在G2/M期(G2 / M phase arrest)及誘導細胞凋亡。同時由西方點墨法(immunobloting) 分析細胞週期素(cyclin A、cyclin B1及cyclin E)，結果顯示蘆薈大黃素對cyclin E無影響，而cyclin A、cyclin B1增加。分析細胞週期素激酶（CDK1及CDK2），CDK1增加而CDK2無影響。另一方面，而引發細胞週期停止在G2/M期之上游因子p27的表現量也會隨著加入蘆薈大黃素而表現量增加，故推論p27也許是調控促使人類前骨髓白血病細胞株發生細胞週期停止在G2/M期的主要因子。流式細胞儀分析實驗與DNA裂解實驗指出，蘆薈大黃素會誘發人類前骨髓白血病細胞株產生凋亡現象(apoptosis)；而且加入10 μM 蘆薈大黃素處理12、24、48與72小時之後，caspase-3的表現量增加。綜合以上之論點得之，蘆薈大黃素的抗癌活性在於抑制人類前骨髓白血病細胞株細胞增殖、引發細胞週期停止在G2/M期與活化caspase-3而促使凋亡發生。; In this study, we have evaluated the chemopreventive role of aloe-emodin in human promyelocytic leukemia (HL-60) cells in vitro by studying the regulation of proliferation, cell cycle and apoptosis. Aloe-emodin inhibited cell proliferation and induced G2/M arrest and apoptosis in HL-60 cells. Investigation on the levels of cyclins B1, E and A by immunoblot analysis showed that cyclin E level was unaffected, whereas cyclin B1 and A levels increased with increasing aloe-emodin in HL-60 cells. Investigation on the levels of cyclin-dependent kinases, Cdk1 and 2, showed that Cdk1 level was increased, where but Cdk2 level was not effected with aloe-emodin in HL-60 cells. The level of p27 was increased after HL-60 cells were cotreated with various concentrations of aloe-emodin. The increase of the levels of p27 may be the major factor for aloe-emodin to cause G2/M arrest in this examined cells. Flow cytometric assays and DNA fragmentation gel electrophoresis also confirmed that aloe-emodin induced apoptosis in HL-60 cells. The level of caspase-3 was increased after HL-60 cells were cotreated with 10 μM aloe-emodin for 12, 24, 48, and 72 hours. Taken together, aloe-emodin therefore appears to exert its anticarcinogenis properties by inhibiting proliferation and inducing cell cycle arrest and apoptosis underwent activation of caspase-3 in human leukemia HL-60 cells.
    显示于类别:[醫學研究所] 博碩士論文

    文件中的档案:

    档案 描述 大小格式浏览次数
    Ch 1.pdf20KbAdobe PDF598检视/开启
    Ch 2.pdf740KbAdobe PDF3599检视/开启
    Ch 3 g.pdf187KbAdobe PDF6478检视/开启
    Ch 4.pdf1544KbAdobe PDF933检视/开启
    Ch 5.pdf28KbAdobe PDF1109检视/开启
    Ch 6.pdf20KbAdobe PDF638检视/开启
    Ch 7.pdf49KbAdobe PDF617检视/开启
    摘要目錄.pdf32KbAdobe PDF972检视/开启
    論文封面-OK.pdf20KbAdobe PDF472检视/开启


    在CMUR中所有的数据项都受到原著作权保护.

    TAIR相关文章

     

    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - 回馈