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作 者:邓守恒[1] 蔡晓军[1] 李芳[1] 李林均[1] 王贤和[1] 陈萍[1]
机构地区:[1]湖北医药学院附属人民医院肿瘤中心,湖北十堰442000
出 处:《时珍国医国药》2013年第5期1230-1232,共3页Lishizhen Medicine and Materia Medica Research
基 金:project supported by the Health Commission of Hubei province of China(grant Nos QJX2008-6);Hubei University of Medicine(grant Nos 2008QDJ1)~~
摘 要:目的观察硒化壳聚糖对体外培养慢性粒细胞白血病多药耐药细胞株K562/ADM细胞生物学行为的影响。方法硒化壳聚糖作用K562/ADM细胞12~24 h,应用流式细胞法检测细胞凋亡,软件拟合计算细胞周期;应用免疫印迹法检测P-gp的表达;应用RT-PCR法检测mdr-1mRNA水平。结果硒化壳聚糖能够明显增强ADM对K562/ADM细胞的诱导凋亡作用,阻滞细胞周期于G1期(P<0.05,P<0.01),下调P-gp表达和mdr-1mRNA水平(P<0.05,P<0.01),硒化壳聚糖浓度越高,作用效果越明显。结论硒化壳聚糖能够通过下调mdr-1基因和P-gp蛋白表达,阻滞细胞于G1期诱导凋亡来对体外培养的K562/ADM细胞耐药生物学行为产生影响。Objective To Investigate the effect of Selenium Chitosan on biological behaviour of human multidrug resistance chronic myelocytic leukemia cell line K562/ADM in vitro. MethodsAfter treated with Selenium Chitosan for 12~24h,the apoptosis rate and cell phase in K562/ADM were examined by flow cytometry.The expression level of P-glycoprotein in K562/ADM was determined by Western Blot and the transcription of mdr-1 gene was detected by semi-quantitative RT-PCR. ResultsSelenium Chitosan could obviously enhance the inducing apoptosis effect of ADM to K562/ADM cell and block cell cycle in G1 phase(P&lt;0.05,P&lt;0.01)、down regulate the abundance of P-glycoprotein and the level of mdr-1mRNA in K562/ADM cell(P&lt;0.05,P&lt;0.01)in a dose dependent manner. ConclusionSelenium Chitosan could change the biological behaviour of K562/ADM cell in vitro through inducing cell apoptosis,blocking cell cycle in G1 phase,inhibiting the expression of P-glycoprotein and mdr-1 gene.
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