CAJ | 학술논문

目的:研究香加皮乙酸乙酯提取物(ethyl acetate extract from Cortex 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IC_(50)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.
목적:연구향가피을산을지제취물(ethyl acetate extract from Cortex periplocae, CPEAE)유도인식관암세포TE-13조망적작용궤제.방법:채용MTT법분석CPEAE대TE-13세포증식적억제작용;Giemsa염색법화투사전자현미경하관찰CPEAE처리후세포조망형태적변화; FCM법검측CPEAE대세포주기화조망솔적영향; Western인적법검측용약전후TE-13세포중CDK4단백표체적변화.결과:CPEAE억제TE-13세포적증식(P<0.05),병정농도급시간의뢰성,작용48 h시적IC_(50)치위(2.443±0.005)μg/mL;투사전자현미경하관찰발현,TE-13세포발생료특정성적조망형태학개변;FCM검측가견전형적조망봉;CPEAE작용TE-13세포후,CDK4기인표체수평강저.결론:CPEAE가유도TE-13세포발생조망,가능시통과하조CDK4기인표체수평이실현적.
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 IC_(50) value was (2.443±0.005) μg/mL at 48 h (P<0.05). 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.