塞来昔布对人白血病细胞株HL-60细胞增殖及凋亡的影响及其作用机制  

Effect of COX-2 Inhibitor Celecoxib on Proliferation,Apoptosis of HL-60 Cells and Its Mechanism

作　　者：谢霞[1] 李杰[1] 王瑞仓[1] 耿瑞丽[1] 王素云[1] 王超[1] 赵晓云[1] 郝洪岭[1] 

机构地区：[1]河北省人民医院血液科,河北石家庄050051

出　　处：《中国实验血液学杂志》2014年第3期707-711,共5页Journal of Experimental Hematology

摘　　要：本研究旨在探讨塞来昔布(celecoxib)对人急性髓系白血病细胞株HL-60细胞增殖、凋亡的影响及其可能的作用机制。不同浓度塞来昔布作用于HL-60细胞24 h后,CCK-8法测定细胞增殖活性,流式细胞技术分析细胞凋亡及细胞周期分布的变化,定量RT-PCR的方法检测细胞周期蛋白D1、E1及COX-2 mRNA的表达。结果表明,不同浓度塞来昔布作用于HL-60细胞24 h后,细胞增殖明显受抑,且呈一定的浓度依赖性(r=0.955),24 h的IC50值为63.037μmol/L。塞来昔布可诱导HL-60细胞的凋亡,也呈剂量依赖性(r=0.988)。塞来昔布可使HL-60细胞明显阻滞于G0/G1期,可下调cyclin D1、cyclin E1 mRNA的表达。塞来昔布可使细胞COX-2 mRNA表达水平降低。结论:塞来昔布呈浓度依赖性抑制HL-60细胞增殖,并可能通过下调cyclinD1、cyclin E1的表达引起细胞G0/G1期阻滞,下调COX-2的表达诱导细胞凋亡。This study was aimed to investigate the effect of COX-2 inhibitor celecoxib on proliferation, apoptosis of human acute myeloid leukemia cell line HL-60 and its mechanism. HL-60 cells were cultured with different concentrations of celecoxib for 24 h. Cell proliferation was analyzed by CCK-8 assay, cell apotosis and cell cycle distribution were detected by flow cytometry. Cyclin D1, cyclin E1 and COX-2 mRNA expressions were determined by RT-PCR. The resuits showed that after the HL-60 cells were treated with different concentrations of celecoxib for 24 h, the cell growth was significantly inhibited in a dose-dependent manner（ r = 0. 955 ）, IC50 was 63. 037 μmol/L of celecoxib. Celecoxib could effectively induce apoptosis in HL-60 cells also in dose-dependent manner（ r =0. 988）, blocked the HL-60 cells in the G0/G1 phase. The expression of cyclin D1, cyclin E1 and COX-2 mRNA were dowuregulated. It is concluded that celecoxib can inhibit the proliferation of HL-60 cells in dose-dependent manner, celecoxib causes cell G0/G1 arrest and induces cell apoptosis possibly through down-regulation of the cyclin D1 and cyclin E1 expression, and down-regulation of COX-2 expression respectively.

关 键 词：白血病 塞来昔布 HL-60细胞 细胞增殖 细胞凋亡 

分 类 号：R733.7[医药卫生—肿瘤]