EGCG协同放射治疗诱导食管鳞癌TE-1细胞凋亡机制的研究
Study on mechanisms of the apoptosis in TE-1 cells of esophageal squamous cell carcinoma induced by EGCG combined with radiotherapy

目的 观察表没食子儿茶素没食子酸酯（EGCG）联合放射治疗（放疗）对食管癌TE-1细胞凋亡的影响，并探讨其分子机制。方法 选择人食管癌细胞株TE-1作为研究对象，并分成对照组、EGCG组、放疗组和联合组（EGCG+放疗）。MTT法检测不同浓度EGCG、不同放射剂量单用和联用对食管癌TE-1细胞生长的影响；流式细胞术检测不同处理组细胞凋亡情况；Western blotting检测经不同处理后TE-1细胞凋亡相关蛋白cleaved caspase-3和抗凋亡蛋白Bcl-2的表达情况。结果EGCG和放疗均能抑制食管癌TE-1细胞的增殖，但EGCG与放疗联合的抑制作用显著高于EGCG组或放疗组（P<0.01），呈浓度-剂量依赖性。流式细胞术检测结果显示，与单独放疗组细胞相比，EGCG联合放疗可以明显提高X射线诱导的TE-1细胞凋亡（P<0.01），上调cleaved caspase-3的表达（P<0.05）和下调Bcl-2蛋白的表达（P<0.05）。结论 EGCG能够协同放疗增加食管癌TE-1细胞的凋亡，这种作用可能与cleaved caspase-3和Bcl-2有关。
： Objective To investigate the effects of epigallocatechin-3-gallate (EGCG) combined with radiotherapy on the apoptosis in TE-1 cells of esophageal squamous cell carcinoma (ESCC) and explore related molecular mechanisms. Methods ESCC TE-1 cells served as subjects and were assigned to the control group, EGCG group, radiotherapy group, and EGCG+radiotherapy group. The effects of different concentrations of EGCG, different doses of radiation, and the combination of EGCG and radiation on the growth of ESCC TE-1 cells were detected by MTT assay. The apoptosis in different treatment groups were measured by flow cytometry. The expression of apoptosis-related proteins including cleaved caspase-3 and anti-apoptosis-related protein Bcl-2 after treatment were detected by Western blotting. Results Both EGCG and radiotherapy inhibited the proliferation of ESCC TE-1 cells. The inhibitory effect of EGCG combined with radiotherapy was significantly higher as compared with the EGCG group or the radiotherapy group in a concentration-dose dependent manner (P<0.01). Results of flow cytometry showed that EGCG combined with radiotherapy significantly increased the apoptosis of TE-1 cells induced by X ray (P<0.01), up-regulated the expression of cleaved caspase-3 (P<0.05), and down-regulated the expression of Bcl-2 (P<0.05) as compared with the radiotherapy group. Conclusion EGCG combined with radiotherapy can increase the apoptosis of ESCC TE-1 cells, which may be associated with cleaved caspase-3 and Bcl-2