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龙葵碱对前列腺癌细胞系PC-3的体外抑制作用
引用本文:章俊,施国伟.龙葵碱对前列腺癌细胞系PC-3的体外抑制作用[J].中华男科学杂志,2011,17(3):284-287.
作者姓名:章俊  施国伟
作者单位:复旦大学附属上海市第五人民医院泌尿外科,上海,200240
摘    要:目的:探讨龙葵碱对雄激素非依赖型人前列腺癌PC-3细胞的体外抑制作用及其机制。方法:分别用0、30、40、50μg/ml浓度的龙葵碱作用PC-3细胞,12、24、48 h后应用CCK-8法检测细胞生长活性、24 h后流式细胞仪测定细胞周期及细胞凋亡变化,荧光显微镜观察细胞凋亡,24 h后应用Western印迹方法检测细胞内IкBα和Bcl-2蛋白的表达。结果:龙葵碱能显著抑制PC-3细胞的生长,呈剂量与时间依赖性,不同浓度龙葵碱组之间与不同作用时间组之间的差异具有显著性意义(P均<0.05)。龙葵碱诱导PC-3细胞出现S期阻滞(P<0.05),各浓度组凋亡细胞比例均高于对照组,差异有显著意义(P均<0.05);不同浓度龙葵碱作用后,可以上调细胞内IкBα蛋白表达,下调Bcl-2蛋白的表达。结论:龙葵碱可以通过抑制PC-3细胞增殖、诱导凋亡、活化PC-3细胞中IкBα蛋白以及抑制Bcl-2蛋白表达等机制发挥抗前列腺癌作用。

关 键 词:龙葵碱  前列腺癌  IкBα  Bcl-2  细胞凋亡

Inbibitory effect of solanine on prostate cancer cell line PC-3 in vitro
ZHANG Jun,SHI Guo-wei.Inbibitory effect of solanine on prostate cancer cell line PC-3 in vitro[J].National Journal of Andrology,2011,17(3):284-287.
Authors:ZHANG Jun  SHI Guo-wei
Institution:Department of Urology,The 5th People's Hospital of Shanghai,Fudan University,Shanghai 200240,China
Abstract:Objective:To investigate the mechanisms of the effects of solanine on human androgen-independent prostate cancer cell line PC-3 in vitro.Methods:PC-3 cells were treated with solanine at the concentration of 0,30,40 and 50 μg/ml,and the cell activity was measured by CCK-8 at 12,24 and 48 hours after the treatment.At 24 hours,the cell cycle and apoptosis were detected by flow cytometry and fluorescence microscopy,and the protein expressions of IкBα and Bcl-2 determined by Western blot.Results:Solanine suppressed the growth of PC-3 cells in a dose-and time-dependent manner in vitro,with significant differences among different concentration and time groups(P0.05).The cycle of the PC-3 cells was arrested in the S phase(P0.05),with a significantly higher rate of apoptosis in the treated groups than in the controls(P0.05).The protein expression of IкBα was obviously up-regulated and that of Bcl-2 down-regulated in all the solanine concentration groups.Conclusion:Solanine has an anti-prostate cancer effect by inhibiting PC-3 cell proliferation,arresting the S phase,inducing cell apoptosis,up-regulating the protein expression of IкBα and down-regulating that of Bcl-2.
Keywords:Bcl-2
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