目的观察根皮素抑制食管癌细胞系EC-109的作用及其可能作用机制。方法采用四甲基偶氮唑盐[3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide,MTT]法观察根皮素对食管癌细胞系EC-109增殖的抑制作用;采用流式细胞仪检测根皮素对食管癌细胞系的凋亡作用的影响;采用酶联免疫吸附试验法(enzyme-linked immuno sorbent assay,ELISA)检测根皮素对食管癌细胞系内B淋巴细胞瘤-2(B-cell leukemia-2,Bcl-2)、B淋巴细胞瘤-2相关蛋白基因(Bcl-2-associated X protein gene,Bax)蛋白表达的影响;采用Western blot法检测根皮素对食管癌细胞系细胞内Bax、Bcl-2、细胞外信号调节激酶(extracellular signal-regulated protein kinases,ERK)及磷酸化细胞外信号调节激酶(phosphorylation of extracelluar signal-regulated kinase,p-ERK)表达的影响。结果根皮素明显抑制食管癌细胞增殖,并且成浓度依赖性。流式细胞仪检测提示根皮素促进食管癌细胞凋亡,与对照组比较差异具有统计学意义(P<0.05)。ELISA及Western blot法提示,根皮素增加食管癌细胞内Bax蛋白表达,抑制Bcl-2蛋白表达,与对照组比较差异具有统计学意义(P<0.05)。Western blot法提示,根皮素抑制细胞内p-ERK蛋白表达,与对照组比较差异具有统计学意义(P<0.05)。结论根皮素明显抑制食管癌细胞增殖,其可能的机制是通过调节ERK信号通路调节细胞凋亡。 Objective To observe the effect of phloretin on inhibiting esophageal carcinoma cell line EC-109 and its possible mechanism. Methods The inhibitory effect of phloretin on the proliferation of esophageal carcinoma cell line EC-109 was observed by MTT method. The effect of phloretin on the apoptosis of esophageal cancer cell lines was detected by flow cytometry. The effects of phloretin on esophageal cancer cell lines were detected by enzyme-linked immunosorbent assay (ELISA) B lymphocyte-2 (Bcl-2) and Bcl-2 protein (Bcl-2), and Western blot Phloretin can inhibit the expression of Bax, Bcl-2, extracellular signal-regulated protein kinase (ERK) and phosphorylation of extracellular signal-regulated kinase (p- ERK) expression. Results Phloretin obviously inhibited the proliferation of esophageal cancer cells in a concentration-dependent manner. Flow cytometry showed that phloretin promoted the apoptosis of esophageal cancer cells, compared with the control group, the difference was statistically significant (P <0.05). ELISA and Western blot suggested that phloretin increased the expression of Bax protein and inhibited the expression of Bcl-2 protein in esophageal cancer cells, which was significantly different from the control group (P <0.05). Western blot suggested that phloretin inhibited the expression of p-ERK protein in the cells, which was significantly different from the control group (P <0.05). Conclusion Phloretin obviously inhibits the proliferation of esophageal cancer cells. Its possible mechanism is that apoptosis is regulated by regulating the ERK signaling pathway.