【作者】 曹琦；

【导师】 韦国桢；

【作者基本信息】 南京医科大学 ， 呼吸内科， 2008， 硕士

【摘要】 目的:了解三氧化二砷对肺腺癌A549细胞株细胞增殖、细胞周期,细胞凋亡以及细胞survivin、cylin D1基因表达的影响。方法:分别以不同浓度的三氧化二砷作用于A549细胞,作用不同时间后对细胞增殖活性、细胞周期、细胞凋亡及细胞survivin、cyclin D1基因表达的变化进行检测。结果:稍高浓度(＞2μmol/L)的三氧化二砷可抑制A549细胞增殖,并呈剂量和时间依赖性。逆转录聚合酶链式反应(RT-PCR)检测survivin、cyclin D1基因转录水平和细胞爬片免疫组化检测survivin、cyclin D1基因蛋白表达的相对强度,发现三氧化二砷作用组survivin和cyclin D1基因的表达与对照组相比明显减低(P＜0.05)。三氧化二砷抑制A549细胞由G1期进入S期结论:三氧化二砷可有效抑制A549细胞增殖,诱导A549细胞凋亡,抑制细胞G1进入S期,并与三氧化二砷剂量和作用时间正相关,这一过程可能与三氧化二砷抑制survivin、cyclin D1表达有关。更多还原

【Abstract】 Objective : To investigat the effect of arsenic trioxide on cell proliferation,cell cycle, cell apoptosis and survivin,cyclin D1 gene expression in lung adenocarcinoma A549 cells. Methods: After A549 were treated with arsenic trioxide in different doses and with different time, MTT was used to detect the proliferation of A549 cells. The Annexin V-FITC /PI double staining analysis by flow cytometry was used to evaluate apoptosis rate. Cell cycle was elaluated by PI staining FCM anlysis. Survivin ,cyclin D1 gene expression was detected by RT-PCR and immunohistochemesitry. Results: Arsenic trioxide could inhibit cell proliferation, induce cell apoptosis and stop cell cycle at G1/S transition in A549 cells. The apoptotic rate was both dose depedent and time dependent. Survivin and cyclin D1 gene expression was down regulated in arsenic trioxide group compared with the control. Conclusion: Arsenic trioxide can effectively inhibit cell proliferatioin and induce apoptosis in lung adenocarcinoma A549 cells,this may result from its actioin of reduce survivin and cyclin D1 gene expression. Arsenic trioxide stop cell cycle at G1 phase in lung adenocarcinoma A549 cells, this may result from its actioin of reduce cyclin D1 gene expression.更多还原