紫杉醇诱导人食管癌细胞凋亡的实验研究

Apoptosis in Human Esophageal Carcinoma Cells Induced by Paclitaxel in vitro

目的:研究紫杉醇诱导人食管癌细胞的凋亡作用,并探讨其诱导凋亡的分子机制。方法:通过形态学观察,流式细胞仪技术分析研究紫杉醇对人食管癌细胞的凋亡作用,免疫组化测定bcl-2、p53、p21在紫杉醇处理前后的变化。结果:紫杉醇作用于Eca109细胞后,可见到较典型的细胞凋亡形态学变化:细胞核固缩、解聚以及凋亡小体。流式细胞仪检测显示,G1峰前有一明显的凋亡峰。免疫组化显示,bcl-2、p53在紫杉醇处理前后无变化,而p21表达增加。结论:紫杉醇可能通过p21诱导人食管癌细胞凋亡。

Objective： To study the effect of paclitaxel on inhibiting human eophageal carcinoma cells and the molecular mechanism of the apoptosis. Methods： The apoptosis of esophageal carcinoma cells and the changes of bcl-2, p53, and p21 were observed morphologically and were analyzed with flow-type cytometry after the treatment with paclitaxel. Results： Typical morphologic changes of apoptosis such as nucleus pyknois, nucleus depolymerization, and apoptic bodies, were found after paclitaxel acting on Ecal09 cells. Flow-type cytometry analysis showed an apoptosis peak before G1. The levels of protein bcl-2 and p53 appeared no change. The level of p21 increased. Conclusion： Paclitaxel can induce apoptosis of Ecal09 cells in human esophageal carcinoma, and p21 plays a possible role in the changes.