舒林酸对结肠癌SW1116细胞生长的影响

目的观察选择性环氧化酶－2（COX－2）抑制剂尼美舒利（nimesulide）与非选择性COX抑制剂舒林酸（sulindac）对结肠癌细胞株SW1116前列腺素E2（PGE2）释放的影响，以及舒林酸对细胞增殖、凋亡、细胞周期的影响，以探讨非甾体抗炎药（NSAIDs）的抗癌机制。方法采用放射免疫法检测尼美舒利和舒林酸作用前后细胞上清液中PGE：水平的变化；四甲基偶氮唑蓝（MTT）比色法观察舒林酸对结肠癌细胞SW1116增殖的抑制作用；流式细胞术（FCM）分析舒林酸对细胞凋亡及细胞周期的影响。结果放免检测发现，尼美舒利、舒林酸作用1h即可出现细胞上清液中PGE2水平下降，且呈剂量依赖性，与对照组相比，差异有统计学意义（P〈0．05）；MTT比色法显示舒林酸呈时间和剂量依赖性抑制细胞的增殖（P〈0．05或P〈0．01）；FCM分析结果显示舒林酸能促进细胞的凋亡且改变细胞周期的分布（降低G0／G1期细胞的比例、增加S期和G2／M期细胞的比例），与对照组相比，差异有统计学意义（P〈0．05或P〈0．01）。结论NSAIDs能抑制结肠癌SW1116细胞的生长，其机制可能与阻滞细胞周期的进程、促进细胞凋亡、抑制PGE2的释放等有关。

Study on the esulindac's effect on the growth of human (SW1116) colon cancer cell

Objective To study the mechanism of non - steroidal anti - inflammatory drugs （NSAIDs） as the chemnprevention and anticancer agents, the effect of selective cyclooxygenase -2 （COX -2） inhibitor nimesulide and non - selective COX inhibitor sulindac have on prostaglandins E2 （ PGE2 ） ＇s release, and the effect of sunlindac on cell proliferation, apoptosis, cell cycle of colon cancer SW1116 cells. Method PGE2 content were examined in the culture supernatant by radioimmunoassay and ELISA method. Methyl thiazolyl tetrazolium （MTT） assay and flow cytometry （FCM） were used to determine the influence of sunlindac on the cell proliferation and cell apoptosis, cell cycle of colon cancer cells. Result Nimesulide and sulindac reduced PGE2 release in a dose - dependent manner. Sulindac increased cells apoptosis rate （P 〈0. 05 or P 〈 0. 01 vs. control） and inhibited cells proliferation in a dose and time-dependent manner （P 〈0. 05 or P 〈 0. 01 ）. And it decreased the proportion of cells in the G0/G1 phase, at the same time, increased the proportion of cells in the S and G2/M phase （P 〈 0. 05 or P 〈0. 01 vs. control）. Conclusions NSAIDs can inhibit proliferation of colon cancer cells, which may be due to that it blocks cell cycle progression and inducing cell apoptosis and down -regulats PGE2 release.