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中国临床药理学与治疗学 ›› 2005, Vol. 10 ›› Issue (1): 61-64.

• 研究原著 • 上一篇    下一篇

NS-398 诱导肝癌细胞凋亡的实验研究

张岭漪, 张有成, 傅生军, 王祥, 马力   

  1. 兰州大学第二医院消化内科, 兰州 730030, 甘肃
  • 收稿日期:2004-09-17 修回日期:2004-12-20 出版日期:2005-01-26 发布日期:2020-11-19
  • 通讯作者: 张岭漪, 女, 硕士, 副教授, 从事消化病专业, 主要研究方向为肝脏病学。Tel:013008780697 E-mail:zhanglymd@yahoo.com.cn
  • 基金资助:
    甘肃省教育厅科研资助项目(No2003-033-06)

Experimental study on apoptosis of HepG2 cell induced by NS-398

ZHANG Ling-yi, ZHANG You-cheng, FU Sheng-jun, WANG Xiang, Ma Li   

  1. Department of Internal Medicine, the Second Hospital of LanzhouUniversity, Lanzhou 730030, Gansu, China
  • Received:2004-09-17 Revised:2004-12-20 Online:2005-01-26 Published:2020-11-19

摘要: 目的: 研究选择性环氧化酶-2(COX-2) 抑制剂NS-398 对人肝癌细胞HepG2 凋亡的影响, 及其相关蛋白Bcl-2 在细胞凋亡中的作用。方法: 通过体外细胞培养, 应用荧光显微镜、透射电镜、流式细胞仪观察NS-398 对HepG2 的凋亡诱导作用, 应用免疫细胞化学法观察Bcl-2 在人肝癌细胞HepG2 凋亡中的表达。结果: NS-398 处理HepG2 细胞后, 电镜下可见到细胞核固缩、染色质凝集成新月型紧靠核膜周边,核碎裂、染色质片断化等典型的细胞凋亡形态变化。荧光显微镜及流式细胞检测则未见凋亡征象。免疫细胞化学分析显示, NS-398 处理后的HepG2 细胞,其Bcl-2 表达较对照组明显下降。结论: COX-2 选择性抑制剂NS-398 对人肝癌HepG2 细胞有显著的凋亡诱导作用;抗凋亡基因Bcl-2 在NS-398 诱导的HepG2 细胞凋亡中有重要的调控作用。

关键词: 肝细胞癌, 环氧化酶-2 抑制剂, NS-398, 凋亡, Bcl-2

Abstract: AIM: To study the effects of selective COX-2 inhibitor NS-398 on apoptosis of HepG2 cell line and to evaluate the modulation activity of Bcl-2 on the procession of HepG2 cell apoptosis.METHODS: HepG2 cells were cultured in RPMI1640 media and treated by NS-398 for 24, 48 and 72 hours.The apoptosis of HepG2 cells was observed by fluorescent microscopy, transmission electronmicroscopy and flow cytometric analysis.The expression of Bcl-2 in HepG2 cells during the apoptosis was measured by immunocellularchemical staining.RESULTS: NS-398 obviously induced some morphologic features of HepG2 cell apoptosis such as cellular nucleus shrinking, nucleus fragments, luniform chromatin agglutinating and chromatin fragmentation.Compared with the control group, the NS-398 group significantly decreased the expression of Bcl-2.CONCLUSION: COX-2 selective inhibitor NS-398 can significantly induce the apoptosis of hepG2 cells, and Bcl-2 may play an important role in modulating apoptosis induced by NS-398.

Key words: hepatic carcinoma, cyclooxygenase-2 inhibitor, NS-398, apoptosis, Bcl-2

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