基础医学与临床 ›› 2020, Vol. 40 ›› Issue (10): 1369-1373.

• 研究论文 • 上一篇    下一篇

去氢木香内酯抑制人肝癌细胞系HepG2增殖及促凋亡

苗加伟1, 陈洁1, 邓雪松1,2, 熊书1,2, 李国利1,2, 马强1,2*   

  1. 1.重庆三峡医药高等专科学校 基础医学部, 重庆 404120;
    2.重庆市抗肿瘤天然药物工程技术研究中心, 重庆 404120
  • 收稿日期:2020-05-06 修回日期:2020-07-29 出版日期:2020-10-05 发布日期:2020-09-29
  • 通讯作者: * cjmaqiang@163.com
  • 基金资助:
    重庆市教育委员会科学技术研究项目(KJQN201802712,KJ1725385,KJQN201902701,KJQN201802711);重庆市自然科学基金(cstc2018jcyjAX0469);重庆三峡医药高等专科学校自然科学基金重点项目(2016xzz03)

Dehydrocostuslactone inhibits proliferation and promotes apoptosis of human hepatocellular carcinoma cell line HepG2

MIAO Jia-wei1, CHEN Jie1, DENG Xue-song1,2, XIONG Shu1,2, LI Guo-li1,2, MA Qiang1,2*   

  1. 1. Department of Basic Medicine, Chongqing Three Gorges Medical College, Chongqing 404120;
    2. Chongqing Engineering Research Center of Antitumor Natural Drugs, Chongqing 404120, China
  • Received:2020-05-06 Revised:2020-07-29 Online:2020-10-05 Published:2020-09-29
  • Contact: * cjmaqiang@163.com

摘要: 目的 研究去氢木香内酯(Dehy)对人肝细胞癌HepG2细胞增殖和凋亡的影响,并对分子机制进行一定的探索。方法 将HepG2细胞分为对照组、Dehy 10、20、30、40及50 μmol/L组。MTT法检测细胞增殖;Hoechst 33258荧光染色检测细胞凋亡;Western blot检测p-IκBα、IκBα、nuclear-p65和total-p65蛋白表达。结果 与对照组相比,Dehy明显呈剂量与时间依赖性抑制HepG2细胞的增殖,并显著诱导HepG2细胞凋亡(P<0.05或P<0.01);p-IκBα、nuclear-p65蛋白表达水平明显下调(P<0.05或P<0.01),IκBα蛋白表达明显上调(P<0.05或P<0.01), 而total-p65未见明显变化。结论 Dehy抑制HepG2细胞增殖和诱导凋亡,其作用机制可能与下调NF-κB通路有关。

关键词: 去氢木香内酯, 肝癌, 核因子-κB, 细胞增殖, 凋亡

Abstract: Objective To investigate the effects of dehydrocostuslactone treatment on the proliferation and apoptosis of human HepG2 cells and potential mechanisms. Methods HepG2 cells were divided into 6 groups incubated with different concentration of Dehydrocostuslactone. The cell proliferation was evaluated by MTT assays, and Hoechst 33258 fluorescence staining was conducted to observe apoptosis of cells subsequently.The expression of p-IκBα, IκBα, nuclear p65 and total p65 proteins in HepG2 cells were measured using Western blot. Results Compared with the control group, dehydrocostuslacton,in a dose dependent manner, significantly inhibited the proliferation of HepG2 cells with impressive profile of apoptosis (P<0.05 or P<0.01). Dehydrocostuslactone, at concentrations of 10, 20 and 30 μmol/L, resulted in a significantly decrease of p-IκBα and nuclear p65 expression (P<0.05 or P<0.01) and an increased IκBα expression (P<0.05 or P<0.01), whereas no marked effect on total p65 expression was observed. Conclusions Dehydrocostuslactone inhibits proliferation and promotes apoptosis of HepG2 cells, the mechanism may be explained by the down-regulation of NF-κB pathway in HepG2 cell.

Key words: dehydrocostuslactone, HepG2 cells, NF-κB pathway, cell proliferation, apoptosis

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