基础医学与临床 ›› 2016, Vol. 36 ›› Issue (9): 1274-1279.

• 研究论文 • 上一篇    下一篇

姜黄素下调PI3K/AKT/mTOR通路抑制人肝癌细胞系增殖

邓进巍1,刘燕1,郭辛翔1,黄波2   

  1. 1. 潍坊市中医院
    2. 中国医学科学院基础医学研究所
  • 收稿日期:2016-05-09 修回日期:2016-07-01 出版日期:2016-09-05 发布日期:2016-08-30
  • 通讯作者: 邓进巍 E-mail:weifangdjw@sina.com

Curcumin inhibits proliferation of human hepatoma cells via down-regulation of PI3K/AKT/mTOR signaling pathway

  • Received:2016-05-09 Revised:2016-07-01 Online:2016-09-05 Published:2016-08-30

摘要: 目的 观察姜黄素对体外培养人肝癌细胞系HL-7702增殖的影响,并探讨其作用机制。方法 体外培养HL-7702细胞,不同浓度的姜黄素(0、10、20、40和80μmol/L)处理48 h。PI3K/AKT抑制剂LY294002联合姜黄素处理细胞。分别用MTT法检测细胞增殖,用Western blot法检测细胞内PI3K、AKT、mTOR、Bax、Bcl-2及活化的caspase-3的蛋白含量。结果 姜黄素可以浓度依赖性的抑制HL-7702细胞增殖,增加细胞中PI3K、AKT和mTOR的磷酸化水平(P<0.05)。姜黄素可诱导HL-7702细胞凋亡,增加Bax和活化的caspase3的含量,减少Bcl-2的含量。LY294002与姜黄素联用后,姜黄素对细胞增殖及凋亡无明显作用。结论 姜黄素可抑制人肝癌细胞系HL-7702增殖,诱导细胞凋亡,作用机制可能与其下调PIK/AKT/mTOR信号通路的活性有关。

关键词: 姜黄素, 人肝癌细胞HL-7702, 增殖, PI3K/AKT/mTOR

Abstract: Objective: The effect of curcumin over human hepatoma cell line HL-7702 proliferation and the inhibitory mechanism were investigated.Methods: HL-7702 cultured in vitro was treated with a gradient concentration of curcumin(0,10,20,40,80μmol/L)for 48h or subjected to combinational treatment of PI3K/AKT inhibitor LY294002 with curcumin. Then MTT was applied to detect cell proliferation and Western blot was used to detect PI3K,AKT,mTOR,Bax,Bcl-2 protein level and caspase-3 activation status.Results: Curcumin inhibited HL-7702 proliferation in a dose-dependent manner via upregulating phosphorylation of PI3K, AKT and mTOR. Curcumin induced apoptosis of HL-7702 cells with increased Bax and caspase3 activation as well as decreased Bcl-2. In addition, LY294002 attenuated the effect of curcumin over cell proliferation and apoptosis. Conclusion: Curcumin inhibited proliferation and triggered apoptosis of human hepatoma cell HL-7702, which may be caused by downregulating PI3K/AKT/mTOR signaling pathway.

Key words: Curcumin, human hepatoma cell HL-7702, proliferation, PI3K/AKT/mTOR