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目的探讨铁剥夺和铁超负荷对白血病细胞株HL-60细胞凋亡的影响及其机制,为临床采用铁剥夺策略治疗或辅助治疗白血病提供理论依据。方法在HL-60细胞培养基中分别加入不同浓度的去铁胺(DFO)或三氯化铁(FeCl3),造成细胞内铁剥夺或铁超负荷状态,采取噻唑蓝(MTT)法、DNA原位末端标记染色法(TUNEL)、免疫组化法检测铁剥夺和铁超负荷状态下HL-60细胞活力、凋亡率、细胞色素C(Cyt C)阳性细胞率。结果 DFO组细胞活力呈明显下降趋势,凋亡率呈显著上升趋势;FeCl3组细胞活力和凋亡率与对照组相比呈下降趋势;DFO组细胞胞浆内Cyt C阳性细胞率与对照组相比明显升高;而FeCl3组细胞浆内Cyt C阳性细胞率与对照组相比无明显差异。结论铁剥夺可促进线粒体释放Cyt C,诱导HL-60细胞凋亡;铁超负荷对线粒体释放Cyt C无直接影响作用。
Objective To investigate the effects and mechanisms of iron deprivation and iron overload on the apoptosis of leukemia cell line HL-60 and to provide a theoretical basis for the clinical treatment of iron-depleted or adjuvant treatment of leukemia. Methods Different concentrations of deferoxamine (DFO) or ferric chloride (FeCl3) were added to HL-60 cell culture medium to induce intracellular iron-deprivation or iron overload. MTT assay, TUNEL staining and immunohistochemistry were used to detect the cell viability, apoptosis rate and Cyt C positive rate of HL-60 cells under iron deprivation and iron overload. Results The cell viability of DFO group decreased significantly and the apoptosis rate increased significantly. The viability and apoptosis rate of FeCl3 group decreased compared with that of control group. The percentage of Cyt C positive cells in DFO group was higher than that of control group Than that of the control group, while there was no significant difference in the ratio of Cyt C positive cells in the cytoplasm of FeCl3 group. Conclusion Iron deprivation can promote the release of Cyt C from mitochondria and induce the apoptosis of HL-60 cells. Iron overload has no direct effect on the release of Cyt C from mitochondria.