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作 者:贾国存[1] 汤有才[2] 李丰益[3] 廖清奎[3]
机构地区:[1]河南郑州市儿童医院血液科,450053 [2]郑州大学第三附属医院 [3]四川大学华西第二医院儿科血液肿瘤研究所
出 处:《中国小儿血液与肿瘤杂志》2007年第5期209-212,共4页Journal of China Pediatric Blood and Cancer
基 金:河南省医学科技创新人才工程项目(项目编号:2002216)
摘 要:目的探讨HL-60细胞铁池改变对凋亡相关基因表达的影响及可能的分子机制。方法实验分组为去铁胺(DFO)组、DFO+三氯化铁组及空白对照组,分别采用钙黄绿素检测HL-60细胞LIP、流式细胞术观察HL-60细胞凋亡和RT-PCR测定HL-60细胞bax、c-myc、rbmRNA表达。结果(1)不同浓度的DFO作用于HL-60细胞后,随培养时间延长及DFO浓度的增加,动态铁池降低,细胞生存率逐渐下降,显示一定的时间剂量依赖性。(2)不同浓度的DFO作用于HL-60不同时间后,细胞凋亡增加,高于对照组(P<0.05)。(3)RT-PCR结果显示,DFO能明显上调c-myc、rb和baxmRNA表达(P<0.05)。结论DFO通过螯合细胞内铁,降低HL-60细胞LIP,诱导细胞凋亡;诱导HL-60细胞凋亡的作用可能与其降低细胞动态铁池,上调细胞凋亡相关基因c-myc、rb、baxmRNA表达密切相关。Objective To explore the effect of iron chelators on expression of apoptosis relating-genes in HL-60 leukemia cells. Methods We used exponentially growing HL-60 and K562 cells ( 1 × 10^6/ml) in experiment. The study groups were divided as following: DFO group, iron + DFO and control group. Following indices were detected which included viability by typanblue, apoptosis by morphological study, flow eytometry (FCM) assay, expression of rb, c-myc, baxmRNAby RT-PCR, The intracellular LIP was measured with a fluorimetrie assay using the metalsensitive probe calcein-AM. Results the expression levels of Rb and c-myc were increased significantly by DFO (50 μmol/L and 100 μmol/L) (P 〈0. 05), but the extent of the increase was predominant when DFO was 100 μmol/L(P 〈0. 01 ). Conclusions The correlation was a negative between cellular LIP and expression of apoptosis-related increasing the expression of HL-60 cells may be one of mechanisms DFO induced apoptosis in leukemia cells.
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