中文摘要：

目的：研究香加皮乙酸乙酯提取物（ethyl acetate extract fromCortex periplocae,CPEAE）诱导人食管癌细胞TE-13凋亡的作用机制。方法：采用MTT法分析CPEAE对TE-13细胞增殖的抑制作用;Giemsa染色法和透射电子显微镜下观察CPEAE处理后细胞凋亡形态的变化;FCM法检测CPEAE对细胞周期和凋亡率的影响;Western印迹法检测用药前后TE-13细胞中CDK4蛋白表达的变化。结果：CPEAE抑制TE-13细胞的增殖（P〈0.05）,并呈浓度及时间依赖性,作用48 h时的IC50值为（2.443±0.005）μg/mL;透射电子显微镜下观察发现,TE-13细胞发生了特征性的凋亡形态学改变;FCM检测可见典型的凋亡峰;CPEAE作用TE-13细胞后,CDK4基因表达水平降低。结论：CPEAE可诱导TE-13细胞发生凋亡,可能是通过下调CDK4基因表达水平而实现的。

英文摘要：

Objective：To investigate the effect of ethyl acetate extract from Cortex periplocae（CPEAE） on apoptosis of human esophageal carcinoma cell line TE-13 and to elucidate its mechanism.Methods：Inhibitory effect of CPEAE on TE-13 proliferation was tested by MTT assay.The morphological changes of cell apoptosis were observed by Giemsa staining and transmission electron microscopy.Cell cycle and apoptotic ratio were tested by flow cytometry（FCM）.The protein expression of CDK4 was observed by Western blotting.Results：CPEAE inhibited proliferation of TE-13 cells in a concentration-dependent and time-dependent manner,and its IC50 value was（2.443±0.005） μg/mL at 48 h（P0.05）.The characteristic morphological changes of apoptosis were observed in TE-13 cells after treatment with CPEAE under transmission microscope.A typical subdiploid peak was detected by flow cytometry.CPEAE decreased the expression of gene CDK4 in TE-13 cells.Conclusion：CPEAE can induce apoptosis of TE-13 cells.The effect is related with down-regulation of CDK4 expression.