基础医学与临床 ›› 2020, Vol. 40 ›› Issue (3): 315-320.

• 研究论文 • 上一篇    下一篇

雷公藤甲素对非小细胞肺癌细胞系A549增殖的抑制和凋亡的诱导

刘倩1*, 汤建华1, 张志华2   

  1. 1.河北北方学院附属第一医院 药学部, 河北 张家口 075000;
    2.河北北方学院附属第一医院 呼吸内科, 河北 张家口 075000
  • 收稿日期:2019-03-26 修回日期:2019-09-30 出版日期:2020-03-05 发布日期:2020-03-02
  • 通讯作者: *nings570@163.com
  • 基金资助:
    2018年度河北省医学科学研究重点课题计划(20180828)

Triptolide inhibits the proliferation and promotes apoptosis of non-small cell lung cancer cell line A549

LIU Qian1*, TANG Jian-hua1, ZHANG Zhi-hua2   

  1. 1. Pharmacy Department;
    2. Department of Respiratory Medicine, the First Affiliated Hospital of Hebei North University, Zhangjiakou 075000, China
  • Received:2019-03-26 Revised:2019-09-30 Online:2020-03-05 Published:2020-03-02
  • Contact: *nings570@163.com

摘要: 目的 探讨雷公藤甲素(TP)通过调控趋化因子受体4(CXCR4)基因表达对人非小细胞肺癌(A549)细胞增殖和凋亡的影响。方法 实验分为4组:对照组、TP组(100 nm/L TP处理细胞)、CXCR4+TP组(转染质粒及TP处理细胞)和NC+TP组(转染空载质粒及TP处理细胞)。RT-qPCR和Western blot检测CXCR4表达以及转染效果;MTT法检测细胞增殖;Annexin Ⅴ-FITC/PI双染色法检测细胞凋亡;Western blot检测增殖及凋亡相关蛋白表达。结果 雷公藤甲素能够抑制A549细胞中CXCR4 mRNA和蛋白的表达(P<0.05)。雷公藤甲素可抑制A549细胞增殖,诱导其凋亡(P<0.05)。转染pcDNA-CXCR4能够上调CXCR4 mRNA和蛋白的表达(P<0.05)。上调CXCR4的表达能够部分逆转雷公藤甲素对A549细胞增殖抑制和凋亡诱导的作用(P<0.05)。结论 雷公藤甲素可能通过下调CXCR4的表达抑制A549细胞增殖,诱导细胞凋亡。

关键词: 雷公藤甲素, CXCR4基因, 非小细胞肺癌细胞系A549, 增殖, 凋亡

Abstract: Objective To investigate the effect of triptolide (TP) on the proliferation and apoptosis of human non-small cell lung cancer cell A549 by regulating the expression of chemokine receptor 4 (CXCR4) gene. Methods The experiment was divided into 4 groups: control group, TP group (100 nm/L TP-treated cells), CXCR4+TP group (transfected plasmid TP-treated cells) and NC+TP group (empty plasmid TP-treated cells). The expression of CXCR4 and transfection were detected by RT-qPCR and Western blot. Cell proliferation was detected by MTT assay, apoptosis was detected by Annexin V-FITC/PI double staining, proliferation and apoptosis-related protein expression were detected by Western blot. Results Triptolide inhibited the expression of CXCR4 mRNA and protein in A549 cells (P<0.05). Triptolide inhibited the proliferation of A549 cells and induced apoptosis(P<0.05). Transfection of pcDNA-CXCR4 up-regulated the expression of CXCR4 mRNA and protein (P<0.05). Up-regulation of CXCR4 expression partially reversed the effect of triptolide on proliferation inhibition and apoptosis induction of A549 cells (P<0.05). Conclusions Triptolide may inhibit the proliferation of non-small cell lung cancer A549 cells and induce apoptosis by down-regulating the expression of CXCR4.

Key words: triptolide, CXCR4 gene, non-small cell lung cancer cell line A549, proliferation, apoptosis

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