目的分析槐定碱抑制食管胃交界腺癌细胞系增殖及诱导凋亡的分子机制。方法采用0~3.0 mg·mL~(-1)质量浓度处理OE~(-1)9和SK-GT2细胞24、48和72 h,分别用CCK-8检测细胞增殖、流式细胞计数检测凋亡和细胞周期、生化分析检测细胞内活性氧(ROS)和谷胱甘肽(GSH)含量、Real-time PCR和Western blot检测FoxM1表达、双荧光素酶报告基因实验检测FoxM1启动子转录活性。结果槐定碱明显抑制食管胃交界腺癌细胞增殖,诱导细胞凋亡,阻滞细胞在G0/G1期,诱导OE~(-1)9细胞内ROS的产生并同时使细胞内GSH含量的减少,其有效作用质量浓度为0.5~1.0 mg·mL~(-1)。此外,槐定碱能够通过抑制FoxM1启动子转录活性而下调FoxM1的mRNA和蛋白表达。结论槐定碱能够通过下调FoxM1基因的表达抑制食管胃交界腺癌细胞的体外增殖。 OBJECTIVE: To study the molecular mechanism of sophoridine in inhibiting proliferation and inducing apoptosis of esophageal-gastric adenocarcinoma cell line. Methods OE ~ (-1) 9 and SK-GT2 cells were treated with 0 ~ 3.0 mg · mL -1 for 24, 48 and 72 h respectively. Cell proliferation was measured by CCK-8 and flow cytometry (ROS) and glutathione (GSH) were detected by biochemical analysis. FoxM1 expression was detected by Real-time PCR and Western blot. The transcriptional activity of FoxM1 promoter was detected by dual luciferase reporter assay. Results Sophoridine significantly inhibited the proliferation of esophageal cancer cells at the junction of esophageal and gastric mucosa, induced cell apoptosis, arrested cells in G0 / G1 phase, induced the production of ROS in OE ~ (-1) 9 cells and reduced the intracellular GSH content , The effective concentration of 0.5 ~ 1.0 mg · mL -1. In addition, sophoridine can down-regulate FoxM1 mRNA and protein expression by inhibiting FoxM1 promoter transcriptional activity. Conclusion Sophoridine can inhibit the proliferation of esophageal and gastric adenocarcinoma cells in vitro by down-regulating FoxM1 gene expression.