江 皓,苏 丹,马胜林.重楼皂甙Ⅰ对肺腺癌细胞株PC9增殖及凋亡的影响[J].肿瘤学杂志,2012,18(3):166-169.
重楼皂甙Ⅰ对肺腺癌细胞株PC9增殖及凋亡的影响
The Effect of Chonglou Saponin I on Proliferation and Apoptosis in Lung Adenocarcinoma Cell Line PC9
投稿时间:2011-11-28  
DOI:10.11735/j.issn.1671-170X.2012.3.B2011551
中文关键词:  肺肿瘤  重楼皂甙Ⅰ  细胞周期  细胞凋亡
英文关键词:lung neoplasms  Chonglou Saponin I  cell cycle  apoptosis
基金项目:浙江省中医药科技计划项目(2011ZZ011);吴阶平医学基金项目(320.6700.09035)
作者单位
江 皓 浙江医院 
苏 丹 浙江省肿瘤医院 
马胜林 杭州市第一人民医院 
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中文摘要:
      摘 要:[目的] 评价重楼皂甙Ⅰ对肺腺癌细胞株PC9增殖和凋亡的影响。[方法] 以体外培养的肺腺癌细胞株PC9为研究对象,MTT法检测重楼皂甙Ⅰ对PC9细胞增殖的抑制作用,流式细胞仪检测重楼皂甙Ⅰ对PC9细胞周期的影响,Annexin-V-FITC/PI 双染法检测重楼皂甙Ⅰ对PC9细胞凋亡的影响,Western blot法检测重楼皂甙Ⅰ对PC9细胞Bcl-2、Bax、caspase-3蛋白表达的影响。[结果] 不同浓度重楼皂甙Ⅰ能有效抑制PC9细胞的增殖,且呈时间浓度依赖性(P<0.01)。2.5μg/ml重楼皂甙Ⅰ作用PC9细胞12h、24h、48h后,出现G2/M期阻滞。2.5μg/ml重楼皂甙Ⅰ作用PC9细胞24h、48h后,细胞凋亡率明显增加,与对照组相比,具有统计学差异(P<0.01)。2.5μg/ml重楼皂甙Ⅰ作用PC9细胞48h后,Bcl-2蛋白表达降低、Bax及caspase-3蛋白表达增加,与对照组相比,亦具有统计学差异(P<0.01)。[结论] 重楼皂甙Ⅰ能抑制PC9细胞的体外增殖,且抑制作用表现出时效和量效关系,其机制可能与G2/M期阻滞、促进细胞凋亡、降低Bcl-2蛋白表达、增加Bax及caspase-3蛋白表达有关。
英文摘要:
      Abstract:[Purpose] To investigate the effect of Chonglou Saponin I on proliferation and apoptosis in lung adenocarcinoma cell line PC9.[Methods] The effect of Chonglou Saponin I on cell prolifera-tion, cell cycle and cell apoptosis were detected by MTT method, FCM and Annexin-V-FITC/PI respectively. The expressions of Bcl-2, Bax and caspase-3 were detected by Western blot.[Results] The growth of PC9 cells was inhibited by Chonglou Saponin I in a dose- and time-dependent manner. After treated with 2.5μg/ml Chonglou Saponin I 12h,24h and 48h, cell cycle was arrested in the G2/M phase. Compared with control group,cell apoptosis was induced significantly(P<0.01) after treated with 2.5μg/ml Chonglou Saponin I at 24h and 48h. The expression of Bcl-2 protein decreased, and the expressions of Bax and caspase-3 protein increased after treated with 2.5μg/ml Chonglou Saponin I at 48h.[Conclusion] Chonglou Saponin I can inhibit cell prolife-ration of lung adenocarcinoma cell line PC9 in a dose- and time- dependent manner.The mechanism might relate to G2/M arrested, inducing cell apoptosis, decreasing expression of Bcl-2, increasing expression of Bax and caspase-3.
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