天然产物研究与开发 ›› 2018, Vol. 30 ›› Issue (5): 847-855.doi: 10.16333/j.1001-6880.2018.5.019

• 开发研究 • 上一篇    下一篇

异甘草素对人肺癌细胞株 H460 增殖、凋亡及NF-κB信号通路的影响

覃月穆1,2,姜泽群1,2,马艳霞2,张旭1,2*   

  1. 1南京中医药大学 医学与生命科学学院;2江苏省中医药防治肿瘤协同创新中心,南京 210023
  • 出版日期:2018-06-04 发布日期:2018-06-04
  • 基金资助:

    江苏省2016年度普通高校研究生科研创新计划(NKY ZZ16_0412);IRSES marie Curie project on China and Europe taking care in health care solutions-CHETCH(PIESES-GA-2013-612589);国家自然科学基金(8160 3584)

Effects of Isoliquiritigenin on Proliferation,Apoptosis and NF-κB Signaling Pathway in Human Lung Cancer H460 Cells

QIN Yue-mu1,2, JIANG Ze-qun1,2, MA Yan-xia2, ZHANG Xu1,2*   

  1. 1School of Medicine and Life Sciences,Nanjing University of Chinese Medicine; 2Jiangsu Collaborative Innovation Center of Traditional Chinese Medicine (TCM) Prevention and Treatment of Tumor,Nanjing University of Chinese Medicine,Nanjing 210023,China
  • Online:2018-06-04 Published:2018-06-04

摘要: 研究异甘草素对人肺癌NCI-H460细胞增殖、周期及凋亡的影响,并探讨其相关分子机制为其治疗肺癌提供新的科学依据。取对数生长期人肺癌NCI-H460细胞,用不同浓度异甘草素处理,采用CCK-8法检测细胞增殖能力;流式细胞术检测细胞周期、凋亡的变化;PCR array 检测肺癌相关基因 mRNA 表达; Western-blot检测 p-p65,IκB α、IκB β、Bax、Bcl-2表达量变化;细胞免疫荧光实验观察异甘草素对 NF-κB p65分布的影响;结果显示,异甘草素能有效抑制人肺癌 H460 细胞的增殖和诱导细胞周期阻滞,并促进其凋亡,其机制可能是通过抑制 NF-κB信号通路的活化,抑制NF-κB p65入核使其不能发挥转录活性,最终影响其下游凋亡相关蛋白 Bax/Bcl-2 的表达来实现的。

关键词: 异甘草素, 肺癌, NCI-H460, 细胞凋亡, NF-&kappa, B

Abstract: To study the effect of Isoliquiritigenin (ISL) on the proliferation,cell cycle and apoptosis of human lung cancer cell line NCI-H460,and to explore its relevant molecular mechanism to provide a new scientific basis for lung cancer treatment.NCI-H460 cells in logarithm growth phase were selected and cultured with different concentration of ISL.The cell viability was detected by CCK-8 assay,while cell cycle and cell apoptosis were measured by cytometry assay.The mRNA expression of lung cancer related genes in NCI-H460 cells were determined by PCR array.The protein levels of p-p65,IκB α、IκB β Bax and Bcl-2 were detected by Western blot analysis.Then,the effect of ISL on the expression of NF-κB p65 was observed by immunofluorescence assay.The results showed that ISL could inhibit proliferation and induce cell cycle block,as well as cell apoptosis in NCI-H460 cells.The mechanism may be related with the inhibition of the NF-κB signaling pathway,by inhibiting the entry of NF-κB p65 into the nucleus,it failing to exert its transcriptional activity and ultimately affecting the expression of downstream apoptotic proteins Bax and Bcl-2.

Key words: isoliquiritigenin, lung cancer, NCI-H460, cell apoptosis, NF-κB

中图分类号: 

R93