文章摘要
张 阳,周康熙,李 俊,耿英华,张 凤,杨艳丽.青蒿琥酯抑制白血病耐药细胞株K562/ADM转铁蛋白受体表达[J].,2017,17(27):5233-5237
青蒿琥酯抑制白血病耐药细胞株K562/ADM转铁蛋白受体表达
Effect of Artesunate on Transferrin Receptor in K562/ADM Cells
投稿时间:2017-03-19  修订日期:2017-04-15
DOI:10.13241/j.cnki.pmb.2017.27.008
中文关键词: 青蒿琥酯  转铁蛋白受体  K562/ADM细胞
英文关键词: Artesunate  Transferrin receptor  K562/ADM cells
基金项目:蚌埠医学院2015年度研究生科研创新计划(Byycx1512)
作者单位E-mail
张 阳 安徽省蚌埠医学院第一附属医院血液科 安徽 蚌埠 233000 gaffet002@163.com 
周康熙 江苏省苏州大学第一附属医院 江苏 苏州 215000  
李 俊 安徽省蚌埠医学院第一附属医院血液科 安徽 蚌埠 233000  
耿英华 安徽省蚌埠医学院第一附属医院血液科 安徽 蚌埠 233000  
张 凤 安徽省蚌埠医学院第一附属医院血液科 安徽 蚌埠 233000  
杨艳丽 安徽省蚌埠医学院第一附属医院血液科 安徽 蚌埠 233000  
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中文摘要:
      摘要 目的:观察青蒿琥酯对于白血病多药耐药细胞细胞株K562/ADM转铁蛋白受体表达的影响。方法:将K562/ADM(耐阿霉素)细胞分别经浓度为12.5、25、50 μg/mL的青蒿琥酯处理48 h,同时25 μg/mL实验组在12 h、24 h、36 h分别收集足量细胞。采用流式细胞术检测青蒿琥酯对细胞转铁蛋白受体(TfR)密度的调控作用,Western blot检测青蒿琥酯对细胞TfR蛋白表达的调控作用。CCK-8法分析青蒿琥酯对K562/ADM细胞生长增殖的影响。结果:K562/ADM细胞TfR密度和TfR蛋白表达水平分别经12.5、25、50 μg/mL 青蒿琥酯处理后均下降,呈浓度依赖性。25 μg/mL青蒿琥酯处理K562/ADM细胞不同时间段后转铁蛋白受体蛋白表达水平随着Art作用时间延长而逐渐降低,表明呈时间依赖性。K562/ADM细胞经青蒿琥酯处理后其耐药性减弱:与对照组相比,12.5、25、50 μg/mL实验组细胞耐药逆转倍数分别为1.38、2.12和2.95倍,从而抑制K562/ADM细胞增殖。IC50值为19.7 μmol/L。结论:青蒿琥酯能降低细胞TfR密度和下调TfR蛋白的表达,逆转K562/ADM细胞的耐药性,从而起到抗肿瘤作用。
英文摘要:
      ABSTRACT Objective: To investigate the effect of Artesunate(Art) on the expression of transferrin receptor(TfR)in K562/ADM cells. Methods: The drug-resistant K562/ADM cells were cultured with 1000 ng/mL doxorubicin for two weeks followed by Artesunate treatment with different concentrations (12.5 μg/mL, 25μg/mL and 50 μg/mL) or different time (12 h, 24 h, 36 h, and 48 h). The content of transferrin receptor in K562/ADM cells was determined by flow cytometry. The effect of Artesunate on the expression of transferrin receptor protein in K562/ADM cells was measured by Western blot. Cell counting kit-8(CCK-8) assay was used to evaluate inhibitory effect of Art combined with doxorubicin (ADM) in K562/ADM cells. The reversal index was defined as the IC50 of the experimental group divided by the IC50 of the control group in K562/ADM cells. Results: Art effectively decreased the content of transferrin receptor and the expression of transferrin receptor protein in K562/ADM cells in a dose-dependent manner. Moreover, Art also inhibited transferrin receptor protein expression in K562/ADM cells in a time-dependent manner. The different concentrations of Art(12.5 μg/mL, 25μg/mL and 50 μg/mL) could induce reversal of drug-resistance with the reversal index being 1.38, 2.12 and 2.95 times (P<0.05). Art inhibited cell proliferation of K562/ADM cells, and the IC50 were19.7 μmol/L. Conclusion: Art effectively down-regulated the transferrin receptor content as well as transferrin receptor protein expression in K562/ADM cells, which resulted in reversal of drug resistance of K562/ADM cells. Art also inhibited K562/ADM cells proliferation, which has great value in clinical treatment of leukemia.
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