摘要
[目的]探讨重楼皂苷Ⅰ(PSⅠ)对胰腺癌PANC-1细胞的放射增敏作用及可能机制。[方法]MTT法检测PSⅠ对PANC-1细胞的增殖抑制作用。克隆形成实验检测PSⅠ对PANC-1细胞的放射增敏效应。流式细胞仪检测细胞周期变化。AnnexinⅤ-PI双染法检测细胞凋亡。Western Blot法检测caspase-3、Bax、Bcl-2蛋白表达改变。[结果]不同浓度PSⅠ对PANC-1细胞有不同程度的体外抑制作用。1μg/ml PSⅠ联合放射线明显降低PANC-1细胞克隆形成率。增敏组凋亡率及G2/M期细胞比例较对照组明显增多(P<0.01)。PSⅠ作用后细胞caspase-3、Bax蛋白表达增加,Bcl-2蛋白表达降低。[结论]PSⅠ对胰腺癌PANC-1细胞具有放射增敏作用,其机制可能与诱导caspase-3、Bax蛋白表达增加,Bcl-2蛋白表达降低,引起细胞G2/M期阻滞,促进细胞凋亡有关。
[Purpose] To investigate the radiosensitization of paris saponin I （ PSI ） on pancreatic carcinoma cell line PANC-1 and its possible mechanism. [Methods] MTF assay was used to measure the effect of PSⅠ on PANC-1 cell proliferation. Clonogenic assay was performed to determine the radiosensitizing effect of PS I on PANC-1 cell line. The cell cycle was measured by flow cytometry and apoptosis was measured by Annexin V-PI. Caspase-3, Bax and Bcl-2 protein expression were detected by Western Blot. [Results]PS I inhibited PANC-1 cell line proliferation. Radiation with PS I （1μg/ml） decreased cloning efficiency significantly. The radiosensitization group had a higher apoptosis rate and G2/M phase cells than control group （P〈 0.01）. Western Blot showed easpase-3 and Bax protein expression increased after the treatment of PSI , but Bcl-2 protein expression decreased. [Conclusion] PSI could enhance the radiosentivity, of pancreatic carcinoma cell line PANC-1 ,which might induce caspase-3, Bax proteins increasing, Bcl-2 protein expression decreasing, and cause G2/M phase arrest and promote cell apoptosis.
出处
《肿瘤学杂志》
CAS
2014年第6期483-487,共5页
Journal of Chinese Oncology
关键词
重楼皂苷Ⅰ
胰腺肿瘤
放射敏感性
paris saponin Ⅰ
pancreatic neoplasms
radiosensitivity
