观察姜黄素对鼻咽癌细胞株C666-1增殖及凋亡的影响，探讨其可能的作用机制。方法：0、10、25、50及100 μmol/L姜黄素作用24 h或50 μmol/L姜黄素不同时间（0、6、12及24 h）后， CCK-8法检测C666-1细胞的增殖情况，TUNEL法检测细胞凋亡，Western blotting检测不同浓度姜黄素作用24 h后细胞内AMPK、S6K1及S6蛋白磷酸化情况。结果：与0 μmol/L 组比，50、100 μmol/L姜黄素作用24 h后，对C666-1细胞增殖的抑制作用显著增强[（38.33±6.53）%、（2114±5.36）% vs （100±0.00）%, 均P<0.05]；50 μmol/L姜黄素作用6 、12 、24 h后，对C666-1细胞增殖的抑制作用显著增强[（49.6±5.67）%、（47.7±6.65）%、（46.86±9.4）% vs （100±0.00）%，均P<0.05]。50、100 μmol/L姜黄素作用后细胞的凋亡率显著增加[（43±12.53）%、（48±8.54）% vs （2.87±1.03)%，均P<0.05]，50 μmol/L姜黄素作用12 、24 h后，细胞凋亡率随作用时间延长而增加[（35.33±5.86）%、（47.33±13.01）% vs (4.33±3.21)%，均P<0.05]。50、100 μmol/L姜黄素可促进细胞内AMPK磷酸化，抑制其下游mTOR信号通路中S6K及S6蛋白的磷酸化活化[（3.87±1.38）、（019±0.16）、（0.39±0.24） vs 1； (4.34±1.34)、(0.059±0.043)、(0.11±0.095) vs 1，均P<0.05]。结论：姜黄素可显著抑制鼻咽癌C666-1细胞增殖和诱导细胞凋亡，其机制可能与影响AMPK、S6K1及S6蛋白磷酸化有关。

To examine the effect of curcumin on mTOR signaling, proliferation and apoptosis in nasopharyngeal carcinoma C666-1 cells in vitro. Methods: C666-1 cells were stimulated by curcumin at increasing concentrations (0, 10, 25, 50, and 100 μmol/L) for 24 h or at a concentration of 50 μmol/L for 0, 6, 12 h and 24 h. Cell proliferation was assessed with the Dojindo’s Cell Counting Kit-8 (CCK-8), cell apoptosis by a TUNEL-based assay and levels of AMPK, S6K, S6 proteins by Western blotting. Results: Curcumin inhibited C666-1 cell proliferation and induced C666-1 cell apoptosis in dose-and time-dependent manners. In parallel with changes in cell proliferation and apoptosis, levels of phosphorylated AMPK were increasing but levels of phosphorylated S6K1 and S6 proteins were decreasing with the dose of curcumin used; against the baseline levels arbitrarily set as 1 in C666-1 cells in the non-treatment control group, the fold of changes in levels of phosphorylated AMPK, S6K1 and S6 proteins was 3.87±1.38, 0.19±0.16 and 0.39±024, respectively, in cells treated with 50 μmol/L for 24 h and was 4.34±1.34, 0.059±0.043 and 0.11±0.095, respectively, in cells treated with 100 μmol/L for 24 h. Conclusion: Curcumin may inhibit nasopharyngeal carcinoma cell proliferation and induce nasopharyngeal carcinoma cell apoptosis through an mTOR signaling pathway-dependent mechanism.

国家自然科学基金资助项目（No. 81302357），广东省自然科学基金资助项目（No. S2013040016493）,广东高校优秀青年创新人才培养计划资助项目（No.2013LYM0075）