5-氨基咪唑-4甲酰胺核苷酸对飚62细胞增殖、分化及凋亡的影响  

Effects of 5-amino imidazole-4formamide nucleotide on proliferation,differentiation and apoptosis in K562 cells

作　　者：王红娟 葛繁梅 刘蕊 张媛媛 Wang Hongjuan;Ge Fanmei;Liu Rui;Zhang Yuanyuan(Department of Hematology and Endocrinology,Xianyang Hospital,Yah'an University,Xianyang 712000,China;Department of Hematology and Immunology,the First Affiliated Hospital,Yan'an University ,Xianyang716000,China)

机构地区：[1]延安大学咸阳医院血液内分泌科,712000 [2]延安大学第一附属医院血液免疫科,咸阳716000

出　　处：《国际免疫学杂志》2018年第6期615-619,共5页International Journal of Immunology

摘　　要：目的 探讨单磷酸腺苷激酶(a monophosphate kinase,AMPK)激动剂5-氨基咪唑-4-甲酰胺核苷酸(5-aminimidazole-4-formamide nucleotide,AICAR)对慢性粒细胞白血病K562细胞株增殖、分化、凋亡的影响.方法CCK-8法检测K562细胞增殖;Wright-Giemsa染色及光学显微镜下观察K562细胞形态;流式细胞仪检测K562细胞表面CD7、CD11b、CD34、HLA-DR表达;FITC Annexin-V/PI双染检测K562细胞早期凋亡;免疫细胞化学法检测野生型P53蛋白表达情况.结果 不同浓度(1.0~2.0 mmol/L)AICAR及不同作用时间(24-72 h)对K562细胞增殖均有抑制作用,并呈时间、剂量依赖性.AICAR可促进野生型p53蛋白的表达.2.0 mmol/LAICAR处理的K562细胞与对照组相比CD7、CD11b、CD34、HLA-DR表面抗原表达无显著差异(P>0.05).结论AICAR对K562细胞增殖抑制作用呈时间和剂量依赖性,其作用机制可能与上调野生型P53蛋白有关.Objective To investigate the effects of 5-aminimidazole-4-formamide nucleotide (AIC-AR),a monophosphate kinase(AMPK)agonist,on proliferation,differentiation and apoptosis of chronic myeloid leukemia K562 cell line. Methods CCK-8 assay was used to detect K562 cell proliferation;Wright-Giemsa staining and light microscopy were used to observe of K562 cell morphology;flow cytometry was used to detect K562 cell surface differentiation antigens CD7,CD11b,CD34,HLA-DR;FITC Annexin-V/ PI double staining was used to detect early apoptosis of K562 cell;and immunocytochemistry was used to detect the expression of wild-type P53 protein. Results AICAR inhibited the proliferation of K562 cells at different concentrations(1. 0~ 2. 0 mmol/ L)and different time(24-72 h),and the inhibition dependented on time and dose. AICAR can pro-mote the expression of wild-type p53 protein. There was no significant difference in the expression of CD7, CD11b,CD34 and HLA-DR surface antigen between K562 cells treated with 2. 0 mmol/ LAICAR and control group(P> 0.05). Conclusion AICAR inhibited the proliferation of K562 cells with time-and dose-dependent . The mechanism may be related to the up-regulation of wild-type P53 protein expression.

关 键 词：5-氨基咪唑4-甲酰胺核苷酸 K562细胞 凋亡 

分 类 号：R965[医药卫生—药理学]