中文摘要：

目的：分析中药香加皮醇提物杠柳苷（periplocin from cortex periplocae，CPP）对食管癌细胞株TE-13的生长抑制作用，探讨其诱导细胞周期阻滞的机制。方法：应用MTr法检测CPP对TE-13细胞的抑制作用；Gimsa染色法分析TE-13细胞的形态学变化；FCM法检测细胞周期分布和凋亡率；Western印迹法检测TE-13细胞经药物处理前后细胞周期蛋白依赖性激酶CDK4、CDK2蛋白表达的变化。结果：CPP对TE-13细胞增殖具有明显的抑制作用（P〈0．01），并呈时间和浓度依赖性，药物浓度越大，作用时间越长，抑制效应越强，CPP作用48h时，对TE-13细胞的半数抑制浓度（IC50）为0．61μg／mL。经2μg／mL的CPP作用48h后，TE-13细胞发生明显的凋亡形态学变化；G0／G1期细胞明显增多（P〈0．01），S期细胞明显减少（P〈0．01），G2／M期细胞没有明显变化（P〉0．05）。不同浓度CPP作用48h后能降低TE-13细胞中CDK4蛋白的表达（P〈0．01），对CDK2蛋白的表达则没有明显影响（P〉0．05）。结论：CPP能显著抑制，TE-13细胞的增殖，其作用机制可能与CPP诱导细胞周期阻滞和细胞凋亡有关。

英文摘要：

Objective： To study the inhibitory effects of periplocin from cortex periplocae （CPP） on proliferation of human esophageal carcinoma TE-13 cells and the related mechanism for cell cycle arrest. Methods： The inhibitory effects of CPP on the growth of TE-13 cells were measured by MTT assay. The morphological changes of TE-13 cells were analyzed by Gimsa staining. Detection of cell apoptosis and cell cycles were performed by flow cytometry. Protein expressions of cyclin-dependent kinase CDK2 and CDK4 were analyzed by Western blotting assay. Results： CPP significantly inhibited the proliferation of TE-13 cells in a dose- and time-dependent manner （ P 〈 0.01 ）. After treatment with CPP for 48 h, the ICs0 was 0.61 la, g/mL. TE-13 cells showed morphologic changes of apoptosis after treatment with CPP 2 μg/mL for 48 h. The proportion of cells in G0/G1 phase significantly increased （P 〈 0.01 ） and the number of cells in S phase decreased （ P 〈0.01 ）. The proportion of cells in G2/M phase had no significant difference before and after CPP treatment （ P 〉 0.05 ）. CDK4 expression was inhibites by CPP at different concentrations, but the expression of CDK2 had no marked changes （P 〉 0.05 ）. Conclusion： CPP significantly inhibites the growth of TE-13 cells. The action mechanism may be related with induction of cell cycle blocking and apoptosis.