首页 | 本学科首页   官方微博 | 高级检索  
检索        

白藜芦醇烟酸酯抑制人肝癌细胞HepG2增殖并诱导细胞的凋亡
引用本文:樊慧婷,熊晓云,曹蔚,高中宝,李小强,贾敏,梅其炳.白藜芦醇烟酸酯抑制人肝癌细胞HepG2增殖并诱导细胞的凋亡[J].中国临床药理学与治疗学,2006,11(5):540-544.
作者姓名:樊慧婷  熊晓云  曹蔚  高中宝  李小强  贾敏  梅其炳
作者单位:1. 第四军医大学药理教研室,西安,710032,陕西
2. 第四军医大学西京医院神经内科,西安,710032,陕西
基金项目:湖北省十堰市科技局资助项目
摘    要:目的:观察白藜芦醇的修饰物白藜芦醇烟酸酯(ResT)对人肝癌细胞HepG2生长增殖的影响及诱导凋亡的作用。方法:用不同浓度的ResT处理HepG2细胞,MTT法检测ResT对HepG2细胞生长增殖的抑制作用;应用Hochest荧光染色法观察凋亡细胞的发生;流式细胞术(FCM)检测分析细胞周期和细胞凋亡率;比色法测定Caspase-3酶活性。结果:ResT抑制HepG2细胞的增殖并呈现一定的量效和时效关系,HepG2细胞与ResT作用后出现典型的凋亡细胞形态改变,FCM分析显示大部分细胞阻滞于G1期,S期细胞比例降低。且药物作用组出现凋亡峰。药物作用12、24、48h后,细胞的凋亡率分别为8.7%、21.1%、和32.7%。显示ResT诱导的细胞凋亡作用随时间的延长而增加,同时Caspase-3酶活性显著增强。结论:ResT可抑制人肝癌细胞HepG2的生长增殖,其作用机制之一可能与阻滞细胞于G1期及诱导细胞凋亡有关。

关 键 词:白藜芦醇  白藜芦醇烟酸酯  细胞凋亡
文章编号:1009-2501(2006)05-0540-05
收稿时间:02 20 2006 12:00AM
修稿时间:03 6 2006 12:00AM

Effects of proliferation inhibition and apoptosis of resveratrol trinicotinate on HepG2 cells and its mechanism
FAN Hui-ting,XIONG Xiao-yun,CAO Wei,GAO Zhong-bao,LI Xiao-qiang,JIA Min,MEI Qi-bing.Effects of proliferation inhibition and apoptosis of resveratrol trinicotinate on HepG2 cells and its mechanism[J].Chinese Journal of Clinical Pharmacology and Therapeutics,2006,11(5):540-544.
Authors:FAN Hui-ting  XIONG Xiao-yun  CAO Wei  GAO Zhong-bao  LI Xiao-qiang  JIA Min  MEI Qi-bing
Abstract:AIM:To study the effects of resveratrol trinocotinate(ResT), a structure modification compound on the basis of resveratrol, on proliferation inhibition and apoptosis in HepG2 cell line. METHODS:HepG2 cell were cultivated with different concentration of ResT at the different time in vitro. The proliferation inhibition was measured by MTT assay. Hochest staining method was used to determine the apoptosis, and then FCM was used to analyzed the cell cycle distribution and apoptosis rate, Colorimetric assay was employed to detect the activation of Caspase-3. RESULTS: ResT caused growth inhibition in a time and dose-dependent manner. After treatment with ResT for 24 h, some cells appeared apoptotic characteristics. The flow cytometric profiles revealed that ResT induced cell into G_1-phase and cells in S-phase were decreased, Apoptotic peaks were observed in the cell cycle analysis. The apoptosis rates were 8.7 %, 21.1 % and 32.7 % respectively after treatment for 12,24,48 h. Caspase-3 was also activated. CONCLUSION:Induction of apoptosis and G_1-phase cell cycle arrest may be responsible for the growth inhibition effect of ResT in HepG2 cell.
Keywords:HepG2  Caspase-3
本文献已被 CNKI 维普 万方数据 等数据库收录!
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号