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柔红霉素对人急性早幼粒细胞白血病细胞株HL-60细胞及干扰素调节因子1、8、9表达的影响
Effect of daunorubicin on the expression of IFN Regulatory Factor 1,-8 and -9 in HL-60 cells

内科 201402期 页码:124-127

作者机构:广西医科大学第一附属医院儿科,南宁市530021

基金信息:(收稿日期:2013-12-26修回日期:2014-02-25)
基金项目:广西壮族自治区科技厅科技攻关项目(桂科攻1140003A-30;桂科能0842009-z8)
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目的研究柔红霉素(Daunorubicin,DNR)对人急性早幼粒细胞白血病(APL)细胞株HL-60细胞中干扰素调节因子1(IRF1)-mRNA、干扰素调节因子8(IRF8)-mRNA、干扰素调节因子9(IRF9)-mRNA表达的影响。方法将HL-60细胞株设为HL-60组、HL-60+DNR组,同时取3例正常人外周血白细胞为NC组。HL-60组为未加药处理组,HL-60+DNR组为小剂量DNR持续作用HL-60细胞10 d。采用实时荧光定量聚合酶链反应(RT-PCR)法检测IRF1-mRNA、IRF8-mRNA、IRF9-mRNA转录水平,每组实验重复3次。结果与NC组相比,IRF1-mRNA、IRF8-mRNA转录水平在HL-60组显著下调(P<0.05),而HL-60+DNR组显著上调(P<0.05);与NC组相比,IRF9-mRNA转录水平在HL-60+DNR显著上调(P<0.05),在HL-60组则表现为下调,但无统计学差异(P>0.05)。结论DNR可上调HL-60细胞中的IRF1、IRF8、IRF9表达水平。APL经DNR治疗后,可能通过上调IRF1、IRF8、IRF9的表达诱导白血病细胞的凋亡,促进其成熟,促进病情的缓解。
ObjectiveTo explore the effect of daunorubicin(DNR) on the expression of IRF1-mRNA, IRF8-mRNA and IRF9-mRNA in acute promyelocytic leukemia cell line of HL-60 cell. MethodsHL-60 cell line was set to HL-60 group, HL-60+DNR group, and the peripheral white blood cells separated from the blood of normal person served as NC group. The HL-60+DNR group was exposed to small doses of DNR every two day for 10 days, while the HL-60 group received no treatment. IRF1-mRNA,IRF8-mRNA and IRF9-mRNA were detected by real-time reverse transcription polymerase chain reaction(RT-PCR). The analysis for each group was performed for three times. ResultsThe expression of IRF1-mRNA and IRF8-mRNA in the HL-60 group were markedly down-regulated compared to the NC group(P<0.05), but were markedly up-regulated in the HL-60+DNR group(P<0.05); compared to the NC group, the expression of IRF9-mRNA in the HL-60+DNR group was markedly up-regulated (P<0.05), and down-regulated in the HL-60 group, but there was no significant difference between the two groups (P>0.05) .ConclusionsDNR can up-regulate the expression of IRF1、IRF8、IRF9 in HL-60 cell line. DNR may induce apoptosis and promote maturation on leukemia cells and promote remission in APL patients.
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