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。
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...
出处
《湖南师范大学学报(医学版)》
2007年第1期15-19,共5页
Journal of Hunan Normal University(Medical Sciences)
基金
湖南省卫生科研项目资助(C2005030)