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山东大学学报（医学版） ›› 2015, Vol. 53 ›› Issue (10): 6-10.doi: 10.6040/j.issn.1671-7554.0.2015.064

• 基础医学 • 上一篇    下一篇

氯化两面针碱对垂体腺瘤GH3细胞的抑制作用

李涛, 吴洪喜, 张永超, 郑志明, 张振, 滕良珠   

  1. 山东大学附属省立医院神经外科, 山东 济南 250021
  • 收稿日期:2015-01-16 出版日期:2015-10-10 发布日期:2015-10-10
  • 通讯作者: 滕良珠。E-mail:tenglz@126.com E-mail:tenglz@126.com
  • 基金资助:
    山东省科技攻关计划(2010GGB14010)

The inhibitory effect of nitidine chloride on pituitary adenoma GH3 cells

LI Tao, WU Hongxi, ZHANG Yongchao, ZHENG Zhiming, ZHANG Zhen, TENG Liangzhu   

  1. Department of Neurosurgery, Provincial Hospital Affiliated to Shandong University, Jinan 250021, Shandong, China
  • Received:2015-01-16 Online:2015-10-10 Published:2015-10-10

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摘要： 目的 探讨氯化两面针碱对垂体腺瘤GH3细胞的抑制作用及其机制。方法 不同浓度的氯化两面针碱作用于GH3细胞,培养不同时间后分别检测其作用效果:CCK-8检测各组GH3细胞存活率;Annexin V/PI凋亡试剂盒染色后,采用流式细胞术检测各组GH3细胞凋亡率;PI染色后采用流式细胞术进行细胞周期分析;实时定量PCR检测凋亡相关基因Bax、 Bcl-2,以及细胞周期相关基因Cyclin B1、CDK1、p21和p27的mRNA表达水平;Western blotting法检测Bax、Bcl-2、Cyclin B1和CDK1蛋白,以及丝氨酸/苏氨酸激酶(AKT)和细胞外信号调节激酶(ERK)信号通路蛋白的表达水平。结果 氯化两面针碱可抑制GH3细胞增殖,促进GH3细胞凋亡及细胞周期阻滞于G2/M期;氯化两面针碱能够抑制AKT及ERK信号通路的激活。结论 氯化两面针碱有效抑制垂体腺瘤GH3细胞的增殖和促进其凋亡,可作为有效治疗垂体腺瘤的潜在药物。

关键词: 凋亡, 丝氨酸/苏氨酸激酶, 氯化两面针碱, 垂体腺瘤, 细胞周期阻滞, 细胞外信号调节激酶

Abstract: Objective To explore the inhibitory effect and role of nitidine chloride on pituitary adenoma GH3 cells. Methods After GH3 cells were treated with different concentrations of nitidine chloride for different periods, cell viability was detected using Cell Counting Kit 8 (CCK8) assay, apoptosis was analyzed using Annexin V/PI Apoptosis Detection kit by flow cytometry, and cell cycle distribution was evaluated using PI staining by flow cytometry. The mRNA expression levels of apoptosis related moleculars Bax and Bcl-2 and cell cycle related moleculars Cyclin B1, CDK1, p21 and p27 were detected with real time PCR. Protein expression levels of Bax, Bcl-2, Cyclin B1, CDK1, activation of AKT signal and ERK signal were determined with Western blotting. Results Nitidine chloride inhibited GH3 cell proliferation, induced apoptosis, arrested cells in G2/M stage, and blocked the activation of AKT and ERK signaling pathway. Conclusion Nitidine chloride inhibits cell proliferation and induces apoptosis of pituitary adenoma GH3 cells. It could be an effective therapeutic agent against pituitary adenoma.

Key words: Nitidine Chloride, Apoptosis, AKT, ERK, Cell cycle, Pituitary adenoma

中图分类号: 

  • R736.4
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