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中国临床药理学与治疗学 ›› 2005, Vol. 10 ›› Issue (5): 505-508.

• 研究原著 • 上一篇    下一篇

硒酸酯多糖诱导白血病多药耐药细胞凋亡的作用机制

张哲文, 魏虎来1, 苏海翔1, 刘建民1, 郝春燕   

  1. 兰州大学基础医学院,1医学实验中心, 兰州 730000, 甘肃
  • 收稿日期:2005-03-21 修回日期:2005-05-08 出版日期:2005-05-26 发布日期:2020-11-19
  • 通讯作者: 魏虎来,男, 研究员, 硕士生导师, 从事细胞分子生物学研究。Tel:0931-8761779 E-mail:weihulai@lzu.edu.cn
  • 作者简介:张哲文, 女, 硕士生, 研究方向:生物化学与分子生物学。
  • 基金资助:
    甘肃省自然科学基金资助项目(NoZR-97-068)

Kappa-selenocarrageenan-induced apoptosis of multidrug-resistant human leukemia cell and its mechanism

ZHANG Zhe-wen, WEI Hu-lai1, SU Hai-xiang1, LIU Jian-min1, HAO Chun-yan   

  1. Basic Medical School,1Labortory Center for Medical Science, Lanzhou University, Lanzhou 730000, Gansu, China
  • Received:2005-03-21 Revised:2005-05-08 Online:2005-05-26 Published:2020-11-19

摘要: 目的: 观察硒酸酯多糖(Kappa-selenocarrag-eenan, KSC) 对 K562/ADM 耐药细胞的诱导凋亡效应, 并探讨其作用机制。方法: 应用噻唑蓝(MTT) 比色法、Wright-Giemsa 染色、DNA 琼脂糖凝胶电泳和流式细胞术(Flow cytometry, FCM) 观察K562/ADM 细胞凋亡;FCM 测定 K562/ADM 细胞 Fas、P53 和 Bcl-2 蛋白表达水平;RT-PCR 检测 Caspase-3 mRNA 的表达。结果: 50 ~ 500 mg°L-1KSC 抑制 K562/ADM 细胞增殖, 并诱导 K562/ADM 细胞凋亡, 细胞出现呈典型凋亡形态改变, DNA 电泳可见 DNA 梯状条带(DNAladder);FCM 分析出现亚 G 1 期细胞群, S 期细胞比例增高。Fas 蛋白表达上调, Bcl-2 蛋白表达下调,Caspase-3 mRNA 表达显著增强, 但 P53 蛋白表达无明显改变。结论: KSC 通过 Fas 依赖性 Caspase-3 激活途径诱导K562/ADM 细胞凋亡。

关键词: 白血病, 多药耐药, 硒酸酯多糖, 凋亡, 机制

Abstract: AIM: To observe the apoptosis of K562 ADM cells induced by kappa-selenocarrageenan(KCS) and to explore its possible molecular mechanism. METHODS: MTT assay, Wright-Giemsa staining, DNA agarose gel electrophoresis and cell-cycle analysis were used for examining apoptosis in K562/ADM cells.Ex-pression of Fas, Bcl-2 and P53 proteins was measured with Flow cytometr(FCM). RP-PCR assay was employed to detect the expression of caspase-3 mRNA. RESULTS: KCS inhibited proliferation of K562/ADM cells.Morpho-logical typical changes of apoptosis were observed through light microscopy. DNA electrophoresis showed evident DNA fragmentation. Cell-cycle analysis indicated in-creased apoptotic cell population (Sub-G1 proportion) as well as apparent S phase arrest. The expression of Fas an-tigens and caspase-3 mRNA significantly increased, and that of Bcl-2 antigens decreased sharply after application of KSC.There was no distinct change of the expression of P53 protein inK562/ADM cells treatedwith KSC.CONCLUSION: KSC induces apoptosis of K562/ADM cells via Fas-caspase-3 pathway.

Key words: leukemia, multi-drug resistance, kap-pa-selenocarrageenan, apoptosis, mechanism

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