5-氨基咪唑-4-甲酰胺核糖核苷酸联合干扰素对K562细胞的影响  

Effect of 5-aminoimidazole-4-formamide Ribonucleotide Combined with Interferon on Chronic Myeloid Leukemia K562 Cells

作　　者：王红娟 刘蕊 张媛媛 葛繁梅[2] WANG Hong-Juan;LIU Rui;ZHANG Yuan-Yuan;GE Fan-Mei(Department of Hematology and Endocrinology,Xianyang Hospital of Yan'an University,Xianyang 712000,Shaanxi Province,China;Department of Hematology and Immunology,The Affiliated Hospital of Yan'an University,716000 Yan'an,Shaanxi Province,China)

机构地区：[1]延安大学咸阳医院血液内分泌科,陕西咸阳712000 [2]延安大学附属医院血液免疫科,陕西延安716000

出　　处：《中国实验血液学杂志》2020年第6期1892-1898,共7页Journal of Experimental Hematology

摘　　要：目的:研究5-氨基咪唑-4-甲酰胺核糖核苷酸(AICAR)联合干扰素(IFN-ɑ-2b)对慢性粒细胞白血病K562细胞的增殖及凋亡的影响,并探讨其可能的作用机制。方法:采用CCK-8法检测细胞增殖抑制情况;Wright-Giemsa方法染色,光学显微镜下观察细胞形态;FITC AnnexinV/PI双染法分析细胞凋亡率的变化;免疫细胞化学法检测野生型P53蛋白的阳性表达率。结果:不同浓度AICAR于不同作用时间24、48和72 h对K562细胞均有抑制作用,抑制程度呈时间、剂量依赖性(r=0.71,r=0.84)。AICAR与IFN-ɑ-2b联合应用后可以有效抑制K562细胞增殖,促进细胞凋亡,联合作用72 h时细胞的抑制率可达(45.26±2.54)%,联合作用48 h早期凋亡率达(33.72±0.23)%,与对照组及单用AICAR和单用IFN-ɑ-2b相比,差异均有统计学意义(P<0.05)。AICAR与IFN-ɑ-2b联合作用促进野生型P53蛋白的表达。结论:AICAR和(或)IFN-ɑ-2b能抑制细胞增殖,促进K562细胞凋亡,2药联合具有协同抗瘤效应,其作用机制可能与促进野生型P53蛋白高表达有关。Objective: To study the effect of 5-aminoimidazole-4-formamide ribonucleotide(AICAR) combined with interferon(IFN-α-2 b) on the proliferation and apoptosis of chronic myeloid leukemia K562 cells,and explore its possible mechanism.Methods: CCK-8 method was used to detect the inhibition of cell proliferation.Wright Giemsa method was used to stain and cell morphology was observed by light microscopy.FITC Annexin V/PI double staining method was used to analyze the change of apoptosis rate.Immunocytochemistry method was used to detect the expression of wild-type P53 protein.Results: Different concentration of AICAR was inhibitory effect on K562 cells at different time point of action for 24 h,48 h,and 72 h,and the inhibition was time and dose-dependent(r = 0.71,r = 0.84).The combination of AICAR and IFN-α-2 b could effectively inhibit the proliferation and promote apoptosis of K562 cells.The inhibition rate of K562 cells was(45.26 ± 2.54) %,and the early apoptosis rate was(33.72 ± 0.23) %,which was statistically significantly different from the control group,AICAR or IFN-α-2b alone(P < 0.05).The combination of two drugs promoted the expression of wild-type p53 protein.Conclusion: AICAR and/or IFN-α-2b can inhibit the cell proliferation and promote the apoptosis of K562 cells.The combination of two drugs shows synergistic antitumor effect,and its mechanism may be related to the promotion of high expression of wild-type p53 protein.

关 键 词：5-氨基咪唑-4-甲酰胺核糖核苷酸 干扰素 K562细胞株 

分 类 号：R733.72[医药卫生—肿瘤]