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铁剥夺抗K562细胞的增殖作用及机制

Mechanism and Antiproliferative Effect of Iron-Deprivation on K562 Cell

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【作者】 汤有才贾国存李丰益廖清奎张冬梅王军

【Author】 TANG You-cai1,JIA Guo-cun2,LI Feng-yi3,LIAO Qing-kui3,ZHANG Dong-mei1,WANG Jun1 (1.Department of Pediatrics,the Third Affiliated Hospital of Zhengzhou University,Zhengzhou 450052,China;2.Department of Hemato-logy, Zhengzhou Children′s Hospital,Zhengzhou 450053,China;3.Institute of Hematology/Oncology, Westchina Second Hospital,Sichuan University,Chengdu 610041,China)

【机构】 郑州大学第三附属医院儿科郑州市儿童医院血液科四川大学华西第二医院血液/肿瘤研究所郑州大学第三附属医院儿科 郑州450052郑州450053成都610041郑州450052

【摘要】 目的观察铁剥夺对白血病细胞增殖的影响。方法以K562细胞作为人类白血病细胞株,台盼蓝染色,光镜下计数活细胞率;用四甲基偶氮唑蓝(MTT)法测A值(570nm),绘制生长曲线;流式细胞术分析细胞周期变化。结果小剂量去铁胺(DFO)(12.5μmol/L)处理K562细胞时,生长曲线轻微变化,随时间延长和DFO剂量增加(25、50、100μmol/L),细胞存活率明显下降,生长曲线高峰显著低于对照组。DFO的抗增殖活性为时间-剂量依赖型。用DFO(50、100μmol/L)处理K562细胞48和72h后,G0/G1期细胞数量增加,S期细胞数量减少,与对照组比较均有显著性差异(Pa<0.001)。上述作用可被等浓度的三氯化铁抵消。结论铁剥夺具有抗白血病细胞增殖作用,剥夺细胞内铁,阻止细胞由G0/G1期进入S期可能是其机制之一。

【Abstract】 Objective To observe the antiproliferative activity of iron-deletion on K562 cell.Methods K562 cell was used as human leukemia cell lines and treated with desferrioxamine in different dosages,the antiproliferative effect of iron-deprivation was observed by methyl thiazolyl tetrazolium(MTT),and the cell cycle analysis was performed by flow cytometry.Results When K562 cells were treated with low-dose desferrioxamine(DFO)(12.5 μmol/L),the growth curve changed slightly,but the peaks of the growth curve were significantly lower than those of control group when K562 cells were treated with mediate-dose(25 μmol/L) and high-dose DFO(50 μmol/L).The antiproliferative activity of DFO increased in a dose dependent manner.The proportion of cells in G0/G1 phase increased and that in S phase decreased,which was significant different from that of control group(Pa<0.001) when K562 cells were treated with DFO(25 μmol/L,50 μmol/L) after 24 and 72 h.Conclusions Iron-deprivation may have antiproliferative activity of leukemic cell.One of the mechanisms may be carried out by chelating intracellular iron and blocking the entrance of cells from G0/G1 to S phase.

【基金】 河南省医学科技创新人才工程项目资助(20022017);河南省科技攻关项目资助(0324410101)
  • 【文献出处】 实用儿科临床杂志 ,Journal of Applied Clinical Pediatrics , 编辑部邮箱 ,2007年03期
  • 【分类号】R363
  • 【被引频次】4
  • 【下载频次】87
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