中文摘要：

目的探讨表没食子儿茶素没食子酸酯（EGCG）对人鼻咽癌CNE-1细胞辐射敏感性的影响及相关机制。方法将细胞分为对照组、EGCG单独处理组、UVC或X射线单独照射组，EGCG联合UVC或X射线照射组。四甲基偶氮唑盐（MTT）比色法检测不同浓度EGCG处理24、48和72h对CNE-1细胞生长的影响，以及EGCG联合紫外线（UVC）及X射线对CNE-1细胞生长的影响。克隆形成实验检测EGCG对CNE-1细胞的放射增敏作用。流式细胞术检测细胞周期变化。AnneXinV．FITC法检测细胞凋亡。WeSternblot法检测相关蛋白表达水平。结果EGCG可抑制CNE-1细胞的生长，并有剂量-效应关系（r=0．817）和处理时间-效应关系（r=0．364）。EGCG在低剂量50μmol／L预处理2h，可增加CNE．1细胞对UVC和X射线的辐射敏感性。相比于单独照射组，EGCG联合UVC照射组细胞的S期阻滞消失（t=18．68，P〈0．05），sub-G．峰的比例则明显增高（t=6．67，P〈0．05）。而且，AnneXinV-FITC检测结果揭示，EGCG联合UVC照射组的细胞中早期凋亡细胞比例显著增加（t=10．28，P〈0．05）。但与单独照射组细胞相比，EGCG联合X射线照射组细胞的S期及G2／M期阻滞更明显（t=7．11和6．99，P〈0．05），无明显的Sub-G，峰出现。EGCG联合UVC照射可使凋亡相关蛋白BaX表达增加（t=5．42，P〈0．05），CaSpaSe-3表达增加（t=4．14，P〈0．05），Bcl-2的表达变化并不明显（t=1．85，P〉0．05），而其联合X射线对于细胞周期相关蛋白Cdc2p34表达的影响不大（t=1．04，P〉0．05）。结论EGCG可抑制鼻咽癌CNE-1细胞的生长。EGCG与UVC联合损伤作用与促进细胞发生早期凋亡相关，涉及到凋亡相关蛋白BaX和CaSpaSe-3；而EGCG和X射线的联合损伤作用可能与周期阻滞相关。

英文摘要：

Objective To investigate the effect of EGCG on the radiosensitivity of human nasopharyngeal carcinoma CNE-1 cells. Methods CNE-1 cells were divided into four groups： control, EGCG treatment, UVC or X-ray exposure, and EGCG combined with UVC or X-rays. After treatment with different concentrations of EGCG for 24, 48 and 72 h and UVC or X- rays, cell growth was determined with MTT assay, cell survival was measured with clonogenic assay, cell cycle was detected with flow cytometry, cell apoptosis was detected by the annexin V-FITC cell apoptosis kit, and protein expression was assayed by Western blot. Results EGCG inhibited cell growth in a dose- and time-dependent manner（r = 0. 817 and 0. 364）. Compared with UVC or X-ray irradiation alone, the radiosensitivity of CNE-1 ceils was enhanced by 2 h pre-treatment of 50 μmol/L EGCG,which disrupted S phase arrest caused by UVC （t = 18.68, P 〈 0.05 ） and increased the population of S and GJM arrest caused by X-rays （ t = 7.11 and 6. 99, P 〈 0. 05 ）. UVC could cause a significant increase of sub-G1 population（ t = 6.67,P 〈 0.05 ） and Annexin V-FITC assay indicated apoptosis was further elevated by EGCG （ t = 10. 28, P 〈 0. 05 ）. However, no significant induction of apoptosis was observed in the ceils either irradiated with X-rays alone orcombinationly treated with EGCG and X-rays. The combination treatment of EGCG and UVC significantly increased the expression of Bax and Caspase-3 proteins, but failed to affect Bcl-2 protein expression. Conclusions EGCG enhances the growth inhibition of CNE-1 cells caused by UVC or X-rays, which is relevant to apoptosis induction or cell cycle arrest.