三氧化二砷联合紫杉醇对A549增殖的影响及机制研究  

Effect of As_2O_3 Combined with Paclitaxel on the Proliferation of A549 Cell and Its Mechanism

作　　者：戴曦 杨小琼 邓述恺 王长安[2] 

机构地区：[1]西南医科大学附属医院呼吸内一科,四川泸州646099 [2]隆昌县人民医院呼吸内科,四川内江642150

出　　处：《四川医学》2017年第9期1014-1017,共4页Sichuan Medical Journal

摘　　要：目的研究三氧化二砷联合紫杉醇对体外培养的肺腺癌A549细胞株的增殖抑制作用及其机制。方法MTT法、克隆实验检测不同干预方式对A549细胞增殖能力的影响;ELISA法检测不同干预方式细胞上清液中COX-2、VEGF含量。结果三氧化二砷和紫杉醇两药联合干预A549时,能抑制A549细胞的增殖并下调COX-2、VEGF表达,与三氧化二砷或紫杉醇单独用药组相比抑制A549细胞增殖差异有统计学意义(P<0.01),并且具有时间依赖性。结论三氧化二砷联合紫杉醇能有效抑制体外培养的人肺腺癌A549细胞株,其机制与下调COX-2和VEGF表达有关。Objective To study the inhibitory action of As2O3 combined with paclitaxel on the proliferation of lung adenocarcinoma A549 cells in vitro and its mechanism. Methods The effects of different interventions on amplification capacity of A549 cells were detected by MTT assay and colony formation test. And ELISA was adopted to determine the contents of COX-2 and VEGF in the supernatant of different interventions. Results As20 3 combined with paclitaxel could inhibit the proliferation of A549 cell and downregulated the expression of COX-2 and VEGF. Compared with As203 or paclitaxel alone, its inhibition of A549 cell＇s proliferation was statistically different （P 〈 0. 01 ）and it＇s time-dependent. Conclusion As 203 combined with paclitaxel can effectively inhibit lung adenocarcinoma A549 cells in vitro and its mechanism is related to downregulation of the expression of COX-2 and VEGF.

关 键 词：三氧化二砷 紫杉醇 肺腺癌 环氧化酶-2 血管表皮生长因子 

分 类 号：R734.2[医药卫生—肿瘤]