中文摘要：

目的：探讨中药香加皮醇提物杠柳苷诱导人食管癌细胞凋亡及其作用机制。方法：应用MTT法检测香加皮醇提物杠柳苷对食管癌细胞TE-13、Eca-109、TE-1和TE-10增殖的影响，并计算其对食管癌细胞的半数抑制浓度（halfinhibitioncon—centration，IC50）；在光学显微镜下观察经杠柳苷处理后细胞的形态学改变；Wright—Giemsa染色观察Eca-109细胞凋亡的形态学变化；FCM检测杠柳苷对Eca-109细胞凋亡的影响；RT—PCR法检测经杠柳苷处理后细胞凋亡相关基因mRNA表达的改变；caspase-3／7蛋白酶活性检测试剂盒检测细胞caspase蛋白酶活性的变化。结果：香加皮醇提物杠柳苷对人食管癌细胞的增殖具有明显的抑制作用；经杠柳苷处理后，Eca-109细胞出现明显的凋亡形态学变化，与未处理组比较，细胞凋亡率明显上升（P〈0．05）；经杠柳苷处理后，Eca-109细胞中survivin和bcl-2mRNA的表达下调（P〈0．05），baxmRNA的表达水平升高（P〈0．05），xiap、caspase-3和caspase-7mRNA的表达水平无明显变化，而caspase-3／7蛋白酶活性明显增加（P〈0．05）。结论：杠柳苷可明显抑制食管癌细胞的增殖，其作用机制可能是通过下调凋亡抑制基因的表达而诱导细胞凋亡。

英文摘要：

Objective ： To study the effect of periplocin （ a sort of ethanol from Cortex periplocae） on apoptosis of human esopha- geal carcinoma cell lines and elucidate its action mechanism. Methods： The proliferation of esophageal cancer cell lines TE-13, Eca- 109, TE-1, and TE-10 were measured using MTF method. The half inhibition concentration （1C50） of periplocin was calculated. Mor- phological changes of esophageal carcinoma cells were observed under light microscope before and after periplocin treatment. The mor- phological features of apoptosis of Eca-109 cells were observed by Giemsa staining. FCM was used to detect apoptotic rate of Eca-109 cells induced by periplocin. Effect of periplocin on mRNA transcription of apoptosis-related genes was determined by RT-PCR assays. Caspase 3/7 activity was detected by caspase Glo 3/7 kit. Results： Periplocin markedly inhibited the proliferation of esophageal cancer cells . After treatment with periplocin, Eca-109 showed apparent apoptotic morphological changes and the apoptosis rate was increased （P 〈 0.05 ）. Expression levels of survivin and bcl-2 mRNA in Eca-109 were down-regulated, but bax mRNA expression was up-regula- ted after periplociu treatment （both P 〈 0.05）. The expression levels of xiap,caspase 3, and caspase 7 mRNA were not changed, but the activity of caspase 3/7 was enhanced significantly as compared to control group （P 〈 0.05 ）. Conclusion ： Periplocin showed very strong inhibitory effects on the proliferation of esophageal carcinoma cells, and the mechanism may be related with down-re-gulation of the expression of apoptosis-suppressor genes and induction of apoptosis.