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中国临床药理学与治疗学 ›› 2017, Vol. 22 ›› Issue (5): 490-494.

• 基础研究 • 上一篇    下一篇

17-DMAG对鼻咽癌细胞株HNE1增殖与凋亡的影响

王 秀1,刘 健2,张竞竞2,朱 娜1,王清清1,李见春1   

  1. 1 蚌埠医学院药学院,蚌埠 233030,安徽;2 蚌埠医学院第一附属医院,蚌埠 233003,安徽
  • 收稿日期:2017-04-13 修回日期:2017-04-25 出版日期:2017-05-26 发布日期:2017-05-27
  • 通讯作者: 李见春,男,博士,副教授,硕士生导师,研究方向:药物新剂型。 Tel: 0552-3150062 E-mail: 541017959@qq.com
  • 作者简介:王秀,女,硕士,讲师,研究方向:生化药理与药物新剂型。 Tel:0552-3150062 E-mail:bbwx1016@163.com
  • 基金资助:

    国家自然科学基金资助项目(81372899);安徽省自然科学基金项目(1608085QH179);安徽省高等学校自然科学研究项目(KJ2015B065by)

17-DMAG inhibits cell growth and induces apoptosis of nasopharynx cancer cell HNE1

WANG Xiu 1, LIU Jian 2, ZHANG Jingjing 2, ZHU Na 1, WANG Qingqing 1, LI Jianchun 1   

  1. 1 School of Pharmacy, Bengbu Medical College, Bengbu 233030, Anhui, China; 2 The First Affiliated Hospital of Bengbu Medical College, Bengbu 233030, Anhui, China
  • Received:2017-04-13 Revised:2017-04-25 Online:2017-05-26 Published:2017-05-27

摘要:

目的: 探讨17-DMAG对鼻咽癌HNE1细胞增殖与凋亡的影响。方法: MTT比色法测定17-DMAG对HNE1细胞活性的影响;溴化丙啶(PI)染色法测定HNE1细胞凋亡;JC-1 染色法测定17-DMAG对线粒体膜电位的影响;Western blot测定细胞Bcl-2/Bax的表达水平。结果: 17-DMAG可抑制鼻咽癌HNE1细胞的增殖,且该抑制作用随作用时间的延长和剂量增加而增强;PI染色显示17-DMAG具有诱导HNE1细胞凋亡作用(P<0.01);JC-1染色显示17-DMAG可诱导HNE1细胞线粒体膜电位降低;Western blot 显示17-DMAG作用HNE1细胞24 h,Bcl-2表达显著降低(P<0.01),Bax表达明显增加,尤其在中、高剂量组(P<0.01)。结论: 17-DMAG具有抑制鼻咽癌细胞HNE1细胞增殖的作用,该抑制作用与浓度和时间成正相关。该作用主要通过诱导HNE1细胞凋亡实现,诱导凋亡的机制可能与其下调细胞线粒体膜电位,降低Bcl-2表达,增加Bax水平有关。

关键词: 17-DMAG, 鼻咽癌, 细胞增殖, 凋亡

Abstract:

AIM: To explore the effect of 17-DMAG on nasopharynx cancer cell proliferation and apoptosis.  METHODS: Cell viability of HNE1 was detected by MTT assay. Cell apoptosis of HNE1 was evaluated by flow cytometry with propidium iodide staining. JC-1 staining was used to determine the effect of 17-DMAG on mitochondrial membrane potential of HNE1 cells. The expressions of Bcl-2 and Bax were detected by Western blot. RESULTS:17-DMAG inhibited the cell proliferation of HNE1 cells in a dose and time-dependent manner. PI staining revealed that 17-DMAG significantly induced HNE1 cell apoptosis(P<0.01). JC-1 staining showed that 17-DMAG reduced the mitochondrial membrane potential of HNE1 cells. Western blot experiment showed that the expression of Bcl-2 decreased significantly (P<0.01). The expression of Bax increased significantly, especially in middle and high dose group after HNE1 cells being treated with 17-DMAG for 24 h (P<0.01). CONCLUSION: 17-DMAG inhibits the growth of HNE1 cells in a dose and time-dependent manner by inducing the apoptosis of HNE1 cells. The mechanism is related with reducing the mitochondrial membrane potential and the expression of Bcl-2, and increases the level of Bax.

Key words: 17-DMAG, nasopharyngeal cancer, cell growth, apoptosis

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