植物性功能食品原料在前列腺癌细胞22RV1中的雄激素效应及其机制研究
作者:
作者单位:

作者简介:

通讯作者:

中图分类号:

基金项目:

国家高技术研究发展计划(863计划,2010AA023001)


Androgenic activities and its mechanism of plant-based functional food ingredients in 22RV1 prostate cancer cells
Author:
Affiliation:

Fund Project:

  • 摘要
  • |
  • 图/表
  • |
  • 访问统计
  • |
  • 参考文献
  • |
  • 相似文献
  • |
  • 引证文献
  • |
  • 资源附件
  • |
  • 文章评论
    摘要:

    目的:研究植物性功能食品原料(当归-甘草-布渣叶)是否具有类雄激素效应,并初步探讨其机制。方法:采用3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium,inner salt(MTS)法检测植物性功能食品原料提取物对雄激素受体阳性前列腺癌细胞22RV1增殖的影响;采用real-time PCR法检测提取物对雄激素受体转录活性的影响。结果:布渣叶提取物与对照组相比,能够促进22RV1细胞的增殖,并且能够诱导雄激素受体靶基因PSA的表达,当加入雄激素受体抑制剂后,细胞活性和PSA水平均明显下降,当归和甘草提取物与对照相比并没有明显改变;ERK1/2的抑制剂U0126也可抑制布渣叶提取物介导的细胞增殖和PSA的表达。结论:在当归-甘草-布渣叶3种植物提取物中,布渣叶具有雄激素效应,并且这种效应依赖雄激素受体途径;ERK1/2信号通路参与了布渣叶提取物介导的雄激素效应。

    Abstract:

    Objective:To investigate the androgenic activities of Microcos paniculata,licorice root,Angelica sinensis and the underlying molecular mechanisms. Methods:The effects of extracts on cell viability were examined by an assay based on 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium,inner salt(MTS). The expression of androgen receptor target gene was determined by real-time PCR. Results:Three extracts were screened for effects on viability of androgen-responsive 22RV1 cells. The extract of Microcos paniculata enhanced cell viability and the expression of PSA mRNA. But they were blocked by the androgen receptor(AR) antagonist flutamide and by the extracellular-signal-regulated kinase 1/2 (ERK1/2) inhibitor,U0126. Conclusion:Microcos paniculata has androgenic activities in an AR-dependent manner among the three plant extracts. And ERK1/2 signaling participates in Microcos paniculata-induced androgenic effects.

    参考文献
    相似文献
    引证文献
引用本文

陆 玲,胡春艳,李 忠,汪之顼.植物性功能食品原料在前列腺癌细胞22RV1中的雄激素效应及其机制研究[J].南京医科大学学报(自然科学版),2013,(7):897-901

复制
分享
文章指标
  • 点击次数:
  • 下载次数:
  • HTML阅读次数:
  • 引用次数:
历史
  • 收稿日期:2013-02-03
  • 最后修改日期:
  • 录用日期:
  • 在线发布日期: 2013-07-09
  • 出版日期:
通知关闭
郑重声明