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目的:探讨重楼皂苷Ⅰ(PPⅠ)对鼻咽癌CNE-2细胞的放射增敏作用及可能机制。方法:MTT法检测PPⅠ对CEN-2细胞增殖抑制作用。克隆形成实验检测PPⅠ对CNE-2的放射增敏效应,单击多靶模型拟合细胞存活曲线并计算放射增敏比。流式细胞仪检测PPⅠ对细胞周期分布和细胞凋亡的影响。结果:PPⅠ对CNE-2细胞有增殖抑制作用,呈时间-剂量依赖性,24和48h半数抑制量(50%concentration of inh ib ition,IC50)分别为6.68μg/mL和3.84μg/mL。1.5和3μg/mL PPⅠ的放射增敏比分别为1.10和1.44,DDP阳性对照组放射增敏比为1.22。增敏组凋亡率、G2/M期细胞比例较对照组增多(P<0.05)。结论:PPⅠ对鼻咽癌细胞系CNE-2具有放射增敏作用,其机制可能与促进细胞凋亡及引起G2/M期阻滞有关。
Objective: To investigate the radiosensitization effect of polysaccharide Ⅰ (PPⅠ) on CNE-2 cells and its possible mechanism. Methods: The inhibitory effect of PPⅠ on the proliferation of CEN-2 cells was detected by MTT assay. The clonogenic assay was used to detect the radiosensitization effect of PPI on CNE-2. The multi-target model was clicked to fit the cell survival curve and the radiosensitization ratio was calculated. Flow cytometry was used to detect the effect of PPⅠ on cell cycle distribution and apoptosis. RESULTS: PPI inhibited the proliferation of CNE-2 cells in a time-and dose-dependent manner. IC50 values were 6.68μg / mL and 3.84μg / mL for 24 and 48 hours, respectively. The radiosensitivities of 1.5 and 3 μg / mL PPI were 1.10 and 1.44, respectively, and the radiosensitivity of DDP positive control group was 1.22. Sensitization group apoptosis rate, G2 / M phase cells increased compared with the control group (P <0.05). CONCLUSION: PPI has radiosensitization effect on CNE-2 cell line CNE-2, which may be related to the promotion of cell apoptosis and G2 / M arrest.