大黄素提升人肝癌细胞活性氧对氟尿嘧啶促凋亡作用的影响  

Influence of emodin on chemotherapeutic drugs induced apoptosis by elevating ROS of human hepatocellular carcinoma cell lines HepG2

作　　者：张利红[1] 官阳[1] 杨木兰[1] 

机构地区：[1]华中科技大学同济医学院病理学系超微病理研究室,湖北武汉430030

出　　处：《医学研究生学报》2007年第8期792-795,共4页Journal of Medical Postgraduates

基　　金：教育部留学回国人员科研启动基金资助项目(批准号:教外司留[2004]479号)

摘　　要：目的：观察大黄素提升人肝癌细胞HepG2活性氧（ROS）水平对氟尿嘧啶（5-FU）促凋亡作用的影响.方法：大黄素以不同方式作用于HepG2细胞,以流式细胞仪（FCM）检测细胞内ROS的动态变化.不同浓度大黄素单用或与5-FU联合作用于HepG2细胞,以MTT检测细胞活力;FCM检测细胞凋亡率及周期分布;透射电镜观察细胞超微结构改变.结果：大黄素剂量和时间依赖性地提升HepG2细胞的ROS水平,2～4h达到高峰.大黄素与5-FU联用,时间及剂量依赖性地增强5-FU对HepG2细胞的促凋亡作用.结论：应用大黄素提升人肝癌细胞HepG2的ROS水平可能是提高化疗药物抗肿瘤疗效的一种手段.Objective： To study the influence of emodin on fluorouracil（5-FU） induced apoptosis by elevating reactive oxygen species（ROS） of human hepatocellular carcinoma cell lines HepG2. Methods： The intracellular ROS levels were detected when exposed to various concentrations of emodin for the indicated periods by flow cytometry（FCM）. MTT assay and FCM were used to assess cell viability, apoptosis and cell cycle distribution after treatment with 5-FU alone or combined with various concentrations of emodin. Transmission electron microscope was applied to observe the uhrastructural change of cells. Results： Emodin elevated intracellular ROS level in a dose- and time-dependent manner, and intracellu- lar ROS level of HepG2 cell incubated in 4 μg/ml emodin reached peak in 2 - 4 h. Emodin combined with 5-FU sensitized HepG2 cell to 5-FU induced apoptosis via generation of ROS in a time- and dose-dependent manner. Conclusion ： Enhancement of ROS generation by emodin may be a novel strategy to improve the curative effect of chemotherapeutic drugs.

关 键 词：大黄素 活性氧 氟尿嘧啶 肝癌细胞 凋亡 

分 类 号：R735.7[医药卫生—肿瘤]