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目的探讨FTY720和雷帕霉素联合用药体外抗胰腺癌细胞增殖的相互作用。方法采用Panc-1和AsPc-1胰腺癌细胞株作为体外研究模型。以不含FTY720或雷帕霉素培养液处理的细胞株为对照组,FTY720单独用药的浓度范围为1～15μmol/L;雷帕霉素单独用药的浓度范围为0.002～200μmol/L,联合用药方案采用两组浓度的雷帕霉素联合7组不同浓度的FTY720;或者采用两组浓度的FTY720联合5组不同浓度的雷帕霉素。采用四甲基偶氮唑盐比色法评估药物对细胞增殖的抑制率,采用双变量相关性分析法统计药物剂量与细胞增殖抑制率之间的相关性。结果单独用药作用下,FTY720或雷帕霉素用药剂量与胰腺癌细胞增殖的抑制率呈现剂量依赖性(FTY720+AsPc-1:r=0.887,P=0.000;雷帕霉素+AsPc-1:r=0.822,P=0.000;FTY720+Panc-1:r=0.796,P=0.000;雷帕霉素+Panc-1:r=0.786,P=0.000)。当10μmol/L FTY720和0.002μmol/L雷帕霉素联用时,对AsPc-1细胞增殖的抑制率达51.8%(P=0.000),对Panc-1细胞增殖的抑制率达37.8%(P=0.000),两药联用具有协同作用。结论FTY720及雷帕霉素在体外均能呈剂量依赖性地抑制胰腺癌细胞增殖,联合用药后能协同抑制胰腺癌细胞的增殖。
Objective To investigate the interaction between FTY720 and rapamycin in the proliferation of pancreatic cancer cells in vitro. Methods Panc-1 and AsPc-1 pancreatic cancer cell lines were used as in vitro models. The cell lines treated with the medium without FTY720 or rapamycin served as the control group, and the concentration of FTY720 alone was 1-15 μmol / L; the concentration of rapamycin alone was 0.002-200 μmol / L, The regimen consisted of two concentrations of rapamycin combined with seven different concentrations of FTY720 or two concentrations of FTY720 combined with five different concentrations of rapamycin. The inhibitory rate of drug on cell proliferation was evaluated by MTT assay. The correlation between drug dose and cell proliferation inhibition rate was calculated by bivariate correlation analysis. Results The FTY720 or rapamycin dose-dependently inhibited the proliferation of pancreatic cancer cells in a dose-dependent manner (FTY720 + AsPc-1: r = 0.887, P = 0.000; rapamycin + AsPc-1: r = 0.822, P = 0.000; FTY720 + Panc-1: r = 0.796, P = 0.000; rapamycin + Panc-1: r = 0.786, P = 0.000). When combined with 10μmol / L FTY720 and 0.002μmol / L rapamycin, the inhibition rate of AsPc-1 cell proliferation was 51.8% (P = 0.000) and the inhibition rate of Panc-1 cell proliferation was 37.8% (P = 0.000), the two drugs synergistic effect. Conclusion Both FTY720 and rapamycin can inhibit the proliferation of pancreatic cancer cells in a dose-dependent manner in vitro, and synergistically inhibit the proliferation of pancreatic cancer cells.