香加皮乙酸乙酯提取物诱导人食管癌TE-13细胞凋亡的作用机制  

Ethyl acetate extract from Cortex periplocae induced apoptosis of human esophageal carcinoma cell line TE-13

作　　者：商晓辉[1] 商晓丽[2] 单保恩[3] 陈育民[1] 任凤芝[4] 刘晓霞[1] 

机构地区：[1]河北工程大学医学院生物教研室,邯郸056029 [2]邯郸市第一医院检验科,邯郸056002 [3]河北医科大学第四医院科研中心,石家庄050011 [4]华北制药集团新药研究开发有限责任公司,石家庄050015

出　　处：《肿瘤》2010年第1期6-10,共5页Tumor

基　　金：国家自然科学基金资助项目(编号:30371753);河北省自然科学基金资助项目(编号:C2004000610)

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。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.

关 键 词：食管肿瘤 香加皮 植物提取物 细胞凋亡 TE-13细胞 

分 类 号：R735.1[医药卫生—肿瘤]