5-氮杂脱氧胞苷对胶质母细胞瘤细胞U87增殖的影响及其机制探讨  

Effect of 5-aza-deoxycytidine on proliferation of glioblastoma U87 cells and the mechanism

作　　者：沈军[1] 邵雪非[1] 徐宗华[1] 江晓春[1] 徐善水[1] 

机构地区：[1]皖南医学院弋矶山医院,安徽芜湖241001

出　　处：《山东医药》2016年第15期8-11,共4页Shandong Medical Journal

基　　金：皖南医学院中青年自然科学基金(WK2014F05)

摘　　要：目的观察5-氮杂脱氧胞苷对胶质母细胞瘤细胞U87增殖的影响,并探讨其可能机制。方法采用不同浓度(0、0.1、0.5、1.0、5、10μmol/L)5-氮杂脱氧胞苷作用于U87细胞,比较细胞增殖抑制率和Bcl-2腺病毒E1B19k Da相关蛋白3 mRNA(BNIP3 mRNA);将5μmol/L的5-氮杂脱氧胞苷作用于U87细胞0、1、2、3、4、5、6 d,比较细胞增殖抑制率及BNIP3 mRNA。将5μmol/L 5-氮杂脱氧胞苷作用于U87细胞4 d,并分别添加和不添加Caspase抑制剂Boc-D-FMK,测算细胞增殖抑制率。结果 5-氮杂脱氧胞苷对U87细胞增殖有抑制作用,且呈剂量及时间依赖性(P均<0.05),抑制作用最强的浓度为5μmol/L,最强的时间点为4 d;Boc-D-FMK并不能抑制由BNIP3所诱导的细胞凋亡,P>0.05。结论 5-氮杂脱氧胞苷可抑制U87细胞增殖,其机制可能与BNIP3 mRNA表达上调有关。Objective To observe the effect of 5-aza-deoxycytidine on the proliferation of glioblastoma U87 cells and to investigate its possible mechanism. Methods Different concentrations of 5-aza-deoxycytidine （5-aza-deo） （0, 0. 1, 0. 5, 1. 0, 5, 10 μmol/L） were used to interfere in the U87 cell line. After 3 days, the inhibition rate of cell proliferation and the BCL2/adenovirus E1B19kDa protein-interacting protein 3 mRNA （BNIP3 mRNA） expression were compared. Af-ter 5 μmol/L 5-aza-deo was used to interfere in U87 cell line at variant time （0, 1, 2, 3, 4, 5 and 6 d）, the inhibition rate of cell proliferation and the BNIP3 mRNA expression were examined. The inhibition rate of cell proliferation was exam-ined after 5 μmol/L 5-aza-deo was used to treat U87 cells for 4 d with Boc-D-FMK or without Boc-D-FMK. Results 5-aza-deo inhibited the U87 cell proliferation which showed a time-and dose-dependent manner （all P〈0. 05）. The concen-tration with the maximum inhibition was 5 μmol/L. The time of maximum inhibition was the 4th day. Boc-D-FMK did not change the apoptosis of U87 cell induced by BNIP3 （P〉0. 05）. Conclusion 5-aza-deo can inhibit the U87 cell prolifer-ation, and its mechanism may be related with the up-regulation of BNIP3 mRNA expression.

关 键 词：5-氮杂脱氧胞苷 胶质母细胞瘤 Bcl-2腺病毒E1B19kDa相关蛋白3 

分 类 号：R739.4[医药卫生—肿瘤]