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龙葵素通过ROS/p38信号通路诱导人前列腺癌细胞凋亡

钟伟枫 陈南辉 黄裕清 万沛 林毅锋 江惠明 钟凯华 潘斌 刘思平

西安交通大学学报(医学版)2017,Vol.38Issue(3):457-461,封3,6.
西安交通大学学报(医学版)2017,Vol.38Issue(3):457-461,封3,6.DOI:10.7652/jdyxb201703025

龙葵素通过ROS/p38信号通路诱导人前列腺癌细胞凋亡

Solanine induces the apoptosis of human prostate cancer cells via ROS/p38 signaling pathway

钟伟枫 1陈南辉 2黄裕清 1万沛 1林毅锋 1江惠明 1钟凯华 1潘斌 1刘思平3

作者信息

  • 1. 广东省梅州市人民医院泌尿外科,广东梅州514021
  • 2. 中山大学肿瘤防治中心泌尿外科,广东广州510060
  • 3. 暨南大学附属第一医院泌尿外科,广东广州 510630
  • 折叠

摘要

Abstract

Objective To investigate the molecular mechanism of solanine-induced apoptosis of prostate cancer cells Du145 and LNCaP.Methods The effects of solanine on the viability of Du145 and LNCaP cells were evaluated by MTT assay.The generation of intracellular reactive oxygen species (ROS) and solanine-induced apoptosis were measured by flow cytometry.The protein levels of p38 and p-p38 expressions were examined by Western blot.Results Solanine significantly inhibited the viability of Du145 and LNCaP cells in a dose-dependent manner (P<0.01).The inhibition of solanine on cell viability was suppressed by the ROS scavenger NAC.ROS generation,apoptosis and phosphorylation of p38 were induced by treatment with solanine at 40 μmol/L for 24 h.The expression of p38 and solanine-induced apoptosis were suppressed by NAC and SB203580.Conclusion Solanine induces the apoptosis of human prostate cancer cell via the RO.S-p38 signaling pathway.

关键词

龙葵素/细胞凋亡/前列腺癌/p38

Key words

solanine/apoptosis/prostate cancer/p38

分类

医药卫生

引用本文复制引用

钟伟枫,陈南辉,黄裕清,万沛,林毅锋,江惠明,钟凯华,潘斌,刘思平..龙葵素通过ROS/p38信号通路诱导人前列腺癌细胞凋亡[J].西安交通大学学报(医学版),2017,38(3):457-461,封3,6.

基金项目

广州市医药卫生科技项目(No.20141A010105) (No.20141A010105)

广东省自然科学基金-博士启动项目(No.2015A030310250) (No.2015A030310250)

中国博士后科学基金面上项目(No.2016M602595)Supported by Medical and Health Science and Technology Project of Guangzhou (No.20141A010105),the Natural Science Foundation of Guangdong Province-Doctoral Startup Project (No.2015A030310250),and China Postdoctoral Science Foundation Grant (No.2016M602595) (No.2016M602595)

西安交通大学学报(医学版)

OA北大核心CSCDCSTPCD

1671-8259

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