文章摘要
黄 耀,姚 欣.新型双芳基脲类化合物对非小细胞肺癌A549细胞的影响[J].南京医科大学学报,2018,(12):1683~1687
新型双芳基脲类化合物对非小细胞肺癌A549细胞的影响
Effects of a new bis⁃aryl urea compound on proliferation,cell cycle and apoptosis of lung cancer A549 cells
投稿时间:2018-03-23  
DOI:10.7655/NYDXBNS20181204
中文关键词: 双芳基脲  化合物N69B  A549细胞  增殖  凋亡
英文关键词: bis⁃aryl urea  bompound N69B  A549 cell  proliferation  apoptosis
基金项目:江苏省兴卫工程(RC201164)
作者单位
黄 耀 南京医科大学第一附属医院呼吸与危重症医学科江苏 南京 210029 
姚 欣 南京医科大学第一附属医院呼吸与危重症医学科江苏 南京 210029 
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中文摘要:
      目的:探讨一种新型双芳基脲类化合物(代号N69B)对非小细胞肺癌A549细胞增殖、周期和凋亡的影响。方法:选择A549非小细胞肺癌细胞系,在不同浓度的N69B作用下,采用CCK?8法测定细胞增殖率、流式细胞仪测定细胞周期变化、Annexin V/PI双染法测定细胞凋亡率、Western blot法测定天冬氨酸特异性半胱氨酸蛋白酶3,8,9活性产物(Cleaved caspase?3,8,9)的相对表达量。结果:与对照组比较,N69B可抑制A549细胞的增殖,且存在明显剂量?效应和时间?效应关系(P < 0.05或P < 0.01);分别采用0.5、1.0和1.5 μmol/L的N69B作用A549细胞24 h后,各药物组G2期细胞比例均显著性升高(P < 0.01);Annexin V/PI双染结果显示,各药物组细胞凋亡率均有不同程度的升高(P < 0.05或P < 0.01);Western blot结果显示,随药物浓度的升高,A549细胞内Cleaved caspase?3、8、9表达量均逐渐升高。 结论:N69B对A549细胞的增殖具有抑制作用,其机制可能与诱导细胞周期G2?M期阻滞及caspase介导的细胞凋亡有关。
英文摘要:
      Objective:To explore anti?cancer activities of a novel bis?aryl urea compound(code name:N69B)using non?small cell lung cancer A549 cells. Methods:The non?small cell lung cancer A549 cells were choosed and treated by N69B at different concentrations. The cell proliferation was quantified by CCK?8 method;the cell cycle was determined by flow cytometry;the apoptosis rate were detected by Annexin V/PI double staining;and the relative expression of Cleaved caspase?3,8,9 was measured by the Western blot. Results:Compared with the DMSO control group,N69B inhibited the proliferation of A549 cells in manners that are time?and dose?dependent(P < 0.05 or P < 0.01). Twenty?four hours after the treatment with N69B at 0.5,1.0 and 1.5 μM,respectively,the number of cells in G2 phase significantly increased(P < 0.01);the apoptosis rate increased in different degrees;Cleaved caspase?3,8,9 expression showed a dose?dependent elevation. Conclusion:N69B inhibits the proliferation of A549 cells,possibly through cell cycle arrest in G2?M phase and apoptosis induced by caspase activation.
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