癌变·畸变·突变 ›› 2003, Vol. 15 ›› Issue (2): 84-87.doi: 10.3969/j.issn.1004-616x.2003.02.007

• 论文 • 上一篇    下一篇

阿克拉霉素对HeLa细胞染色体形成及细胞凋亡的影响

郑全辉, 阴梅云, 郑力芬, 韩 硕, 阎蕴力   

  1. 河北医科大学基础所细胞生物室, 河北 石家庄 050017
  • 收稿日期:2002-05-13 修回日期:2002-06-13 出版日期:2003-04-30 发布日期:2003-04-30
  • 通讯作者: 郑全辉

THE EFFECTS OF ACLARUBICIN ON THE CHROMOSOME FORMATION OF HELA CELL AND APOPTOSIS

ZHENG Quan-hui, YIN Mei-yun, ZHENG Li-fen, et al.   

  1. Insititute of Basic Medicine, Hebei Medical University, Shijiazhuang 050017 , China
  • Received:2002-05-13 Revised:2002-06-13 Online:2003-04-30 Published:2003-04-30
  • Contact: ZHENG Quan-hui

摘要: 目的: 探讨阿克拉霉素对HeLa细胞染色体形成的影响机制及与细胞凋亡的关系。 方法: MTT方法测定阿克拉霉素对HeLa细胞的IC 50值。不同浓度阿克拉霉素作用于HeLa细胞24 h后,制备染色体,Giemsa染色,观察;应用吖啶橙和嗅乙啶双荧光染色及DNA凝胶电泳检测细胞凋亡;Western-blot分析半胱氨酸蛋白酶-3(caspase-3)含量变化。 结果: 阿克拉霉素对HeLa细胞的IC 50值为6.83 μg / ml。染色体分析表明,阿克拉霉素作用于HeLa细胞一定时间后,染色体不规则凝集,正常M期染色体形成受阻。细胞凋亡检测可见10 μg / ml药物组与0.1 μg / ml组及对照组相比,差异显著。Western-blot分析表明,10 μg / ml药物组caspase-3表达比0.1 μg / ml组和对照组显著增加。 结论: 阿克拉霉素能够阻止HeLa细胞染色体形成与分离,导致细胞G 2 / M期阻滞,诱导细胞凋亡。caspase-3在HeLa细胞凋亡中发挥重要作用。

关键词: 阿克拉霉素, 染色质凝集, 细胞凋亡, 半胱氨酸蛋白酶-3

Abstract: Purpose: To investigate the mechanism of chromosome formation of HeLa cell line induced by aclarubicin and the relationship of aclarubicin to apoptosis. Methods: MTT assay was used to detect the half-inhibition concentration (IC 50) of aclarubicin on HeLa cell line, then aclarubicin with different concentrations was chosen to treat HeLa cells for 24 hours, and the nuclei and chromosomes were stained with Giemsastain. Apoptosis of HeLa cell was detected with acridine orange and ethidium bromide(AO / EB) double fluorescence stain and agarose gel electrophoresis. Caspase-3 was assessed with western blot method. Results: After HeLa cells were treated with aclarubicin, the IC 50 was 6.83 μg / ml. The normal chromosome formation was blocked and chromatin condensed disorderly. Apoptosis and DNA fragments were apparent in the 10 μg / ml group. The caspase-3 content in the 10 μg / ml group also showed a marked increase compared with the control and the 0.1 μg / ml group. Conclusion: Aclarubicin can inhibit the normal chromatin condensation and induce the cells G 2 / M arrest, and causes apoptosis. Caspase-3 may play an important role in apoptosis of HeLa cells induced by aclarubicin.

Key words: aclarubicin (ACR), chromatin condensation, apoptosis, caspase-3