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6,8-二-三氟甲基-7-乙酰氧基白杨素抑制酪蛋白激酶诱导人卵巢癌CoC1细胞凋亡
引用本文:刘华清,秦勇,张燕琴,夏红,董琳,曹建国. 6,8-二-三氟甲基-7-乙酰氧基白杨素抑制酪蛋白激酶诱导人卵巢癌CoC1细胞凋亡[J]. 湖南师范大学学报(医学版), 2007, 4(1): 15-19
作者姓名:刘华清  秦勇  张燕琴  夏红  董琳  曹建国
作者单位:南华大学肿瘤研究所,南华大学药物药理研究所,湖南,衡阳,421001
基金项目:湖南省卫生科研项目资助(C2005030)
摘    要:目的:研究6,8-二-三氟甲基-7-乙酰氧基白杨素(9dFMAChR))抑制体外培养人卵巢癌细胞系CoC1细胞增殖和诱导凋亡作用及机制。方法:体外培养CoC1细胞,MTT比色法测定dFMAChR对CoC1细胞增殖活性的影响;AO/EB染色法荧光显微镜观察dFMAChR诱导CoC1凋亡细胞的形态学改变;DNA凝胶电泳确证dFMAChR诱导CoC1细胞凋亡作用;Western blotting法分析dFMAChR对CoC1细胞酪蛋白激酶CK2α蛋白表达和活性的影响。结果:MTT比色法结果显示,dFMAChR有效抑制CoC1细胞增殖活性,呈剂量依赖性;其IC50值为11.8μM。AO/EB染色荧光显微镜观察dFMAChR处理后,部分CoC1细胞呈现典型凋亡细胞形态特征;dFMAChR(10.0μM)处理CoC1细胞48 h,琼脂糖凝胶电泳出现“梯形”DNA条带。Western blotting分析结果表明:dFMAChR下调酪蛋白激酶CK2α表达,呈浓度和时间依赖性。结论:dFMAChR具有抑制人卵巢癌CoC1细胞增殖和诱导细胞凋亡作用;作用机制与其抑制酪蛋白激酶CK2α表达有关。

关 键 词:卵巢癌  白杨素  6,8-二-三氟甲基-7-乙酰氧基白杨素  酪蛋白激酶  细胞凋亡
文章编号:1673-016x(2007)01-0015-06
修稿时间:2006-12-12

Induction of Apoptosis in Human Ovarian Cancer CoC1 Cells through Inhibition of CK2α by 6, 8-ditrifluoromethy -7-acetoychrysin,a Novel Chrysin Derivatives
LIU Hua-Qing,QIN Yong,DONG Lin,ZhANG Yan-Qin,XIA Hong,CAO Jian-Guo. Induction of Apoptosis in Human Ovarian Cancer CoC1 Cells through Inhibition of CK2α by 6, 8-ditrifluoromethy -7-acetoychrysin,a Novel Chrysin Derivatives[J]. Journal of Hunan Normal University(Medical Science), 2007, 4(1): 15-19
Authors:LIU Hua-Qing  QIN Yong  DONG Lin  ZhANG Yan-Qin  XIA Hong  CAO Jian-Guo
Abstract:Objective To investigate the effect and mechanism of 6,8-ditriFluoromethy-7-acetoychrysin(dFMAChR),a novel chrysin derivatives,on the proliferation and apoptosis of human ovarian cancer(CoC1) cell line in vitro.Methods CoC1 cells was cultured in vitro.MTT assay was used to determine the effect of dFMAChR on the proliferation of CoC1 cells.AO/EB fluorescence staining was used to observed the morphologic changes of apoptosis induced by dFMAChR in CoC1 cell line.DNA agarose gel electrophoresis was used to test apotosis induced by dFMAChR in CoC1 cell line.Western blot was used to analyze expression of CK2α protein in CoC1 cells.Results dFMAChR significantly suppressed proliferation of CoC1 cell line in a dose-dependant manner and its IC50 was 11.8 μM.Typical morphologic changes of apoptosis could be observed after treatment with dFMAChR by fluorescence microscope using AO/EB fluorescence staining.DNA agarose gel electrophoresis shown that DNA ladder bands could appear after treatment with dFMAChR at 10 μM for 48h.Western blotting indicated that expression of CK2α protein decreased in a dose-and time-dependent manner.Conclusion dFMAChR could inhibit proliferation and induce apotosis of human ovarian cancer CoC1 cells and its mechanism might be associated with the suppress of expression of CK2α protein.
Keywords:ovarian cancer  Chrysin  6,8-ditrifluoromethy-7-acetoychrysin  CK2α  apoptosis
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