EGCG诱导胃癌和肝癌细胞凋亡及bcl-2表达下调的研究

EGCG induced apoptosis and expression change of bcl-2 protein in gastric and hepatic carcinoma cells

目的：探讨表没食子儿茶素投食子酸酯[（－）－epigallocatechin-3-gallate，EGCG]诱导胃癌MGC－803细胞和肝癌BEL－7402细胞凋亡的作用及其调亡相关基因bcl-2产物表达的改变。方法：用MTT法、琼脂糖凝胶电泳、流式细胞术检测EGCG处理MGC-803细胞和BEL-7402细胞后，他们在形态学和生化方面的改变以及bcl－2蛋白表达水平的变化。结果：EGCG以剂量依赖的方式抑制MGC－803细胞和BEL－7402细胞的生长，其IC50值分别为188．52和264．53μg／ml。200～300μg／ml的EGCG处理MGC-803细胞和BEL-7402细胞24～36h，在琼脂糖凝胶电泳上可见凋亡细胞特征性的“梯状”带和PI染色流式细胞仪直方图上可见亚二倍体峰；流式细胞术显示EGCG以时间依赖的方式下调bcl-2蛋白的表达。结论：EGCG对胃癌MGC-803细胞和肝癌BEL-7402细胞生长具有抑制作用，其机制之一是诱导这两株肿瘤细胞的凋亡。诱导细胞凋亡的机制可能与其下调bcl-2蛋白的表达水平有关。

Objective: To investigate whether (-) - epigallocatechi n- 3 -gallate (ECCG) could induce apoptosi s and affect apoptosis - associated gene bc1-2 expression in gastric carcinoma MGC-803 cells and hepatic carcinoma BEL-7402 cells. Methods: Growth suppression, apoptosis-related alterations in morphology and biochemistry, and change in expression of bc1-2 were determined after EGCG treatment for MGC-803 and BEL-7402 cell lines by using tetrazolium salt MTh assay, gel electrophoresis and flow cytometry. Results: EGCG inhibited the growth of MGC-803 cells and BEL-7402 cells in a dose-dependent manner, with IC50 values of 188. 52 and 264. 53 pg/ml, respectively. Treatment of MGC-803 cells and BEL-7402 cells with 200 ~ 300 μg/ml EGCG for 24 ~ 36 h resulted in apoptosis-associated alterations: 'ladder'bands on agarose gel electrophoresis and hypodiploid peaks on flow cytometric histogram. Moreover, EGCG downregulated bc1-2 expression in MGC-803 cells and BEL-7402 cells with time-dependence. Conclusion: EGCG has the inhibitory effects on the growth of gastric carcinoma MGC-803 cells andhepatic carcinoma BEL-7402 cells, and one of the mechanisms could be the induction of apoptosis in the two tumor cell lines.The apoptosis is associated with GCG-induced decrease of the bc1-2 protein level in MGC-803 and BEL-7402 cell lines.