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目的观察表没食子儿茶素没食子酸酯(EGCG)体外增强阿霉素(ADM)对食管癌CaEs-17细胞化疗敏感性的作用,并探讨可能的作用机制。方法实验分为空白对照组、ADM组(培养液中ADM终浓度为0.3μmol/L),EGCG组(培养液中EGCG终浓度为20 mg/L)、联合组(培养液中EGCG终浓度为20 mg/L,ADM浓度为0.3μmol/L),各组作用24 h,CCK-8法和细胞克隆形成法检测细胞增殖抑制率和存活率,金氏公式评价二药的协同效果;流式细胞仪检测细胞凋亡率及周期分布;Transwell法检测细胞侵袭力;免疫印迹法检测Bax蛋白表达水平。结果 EGCG、ADM均可抑制CaEs-17细胞增殖、诱导细胞凋亡、降低细胞存活率和侵袭力;EGCG、ADM均可阻滞细胞于G0/G1期,并能上调Bax蛋白表达水平(P<0.05),二药联用上述作用效果更为显著(P<0.01)。结论 EGCG能够增强ADM对食管癌CaEs-17细胞的化疗敏感性,这种作用部分是通过上调Bax蛋白实现的。
Objective To observe the effect of epigallocatechin-3-gallate (EGCG) on chemosensitivity of esophageal carcinoma CaEs-17 cells in vitro and to explore its possible mechanism. Methods The experiment was divided into blank control group, ADM group (final concentration of ADM in culture medium was 0.3μmol / L), EGCG group (final concentration of EGCG in culture medium was 20 mg / L), combined group 20 mg / L, and ADM concentration 0.3 μmol / L) for 24 h. CCK-8 and cell clone formation assay were used to detect the cell proliferation inhibitory rate and survival rate. Jin’s formula was used to evaluate the synergistic effect of the two drugs. Cell apoptosis rate and cell cycle distribution were detected by flow cytometry. Cell invasion was detected by Transwell assay. Bax protein expression was detected by Western blotting. Results Both EGCG and ADM could inhibit the proliferation of CaEs-17 cells, induce cell apoptosis, decrease cell viability and invasiveness. Both EGCG and ADM could block cells in G0 / G1 phase and up-regulate Bax protein expression (P < 0.05). The combined effect of the two drugs was more significant (P <0.01). Conclusion EGCG can enhance the chemosensitivity of esophageal carcinoma CaEs-17 cells induced by ADM. This effect is partially achieved through the up-regulation of Bax protein.