NS-398对HepG2细胞增殖的抑制作用及机制探讨  

Inhibition effect and mechanisin of NS-398 on HepG2 cell proliferation

作　　者：彭军[1] 吴青[1] 吴银侠[1] 

机构地区：[1]武汉科技大学附属医院,湖北武汉430064

出　　处：《山东医药》2008年第47期1-3,共3页Shandong Medical Journal

基　　金：湖北教育厅基金项目(D200511008)

摘　　要：目的探讨氮-2,环己氧-4,硝基苯—甲基磺胺(NS-398)对肝癌细胞株HepG2细胞的生长抑制作用及其机制。方法分别用100、200、300、400μmol/L的NS-398处理HepG2细胞,用MTT法测算肿瘤细胞抑制率,流式细胞仪检测细胞周期及细胞凋亡率,用免疫组化和Westernblot检测细胞的血管生长因子(VEGF)。结果NS-398呈剂量依赖性的方式抑制HepG2细胞增殖,并诱导其凋亡,随着NS-398浓度增大,S期细胞明显减少,有G1期细胞累积现象,其24h半数有效剂量(IC50)为300μmol/L。NS-398浓度为200μmol/L以上时HepG2细胞VEGF的表达与对照组相比,P<0.01。结论NS-398对肝癌细胞增殖有抑制作用,并诱导其凋亡,可能与G1阻滞以及VEGF的表达受抑制有关。Objective To invesigate inhibition effect and mechanism of NS-398 on HepG2 cells. Methods HepG2 cells were treated with various concentrations（ 100,200,300,400μmol/L） of NS-398. MTr method was used to detect cell proliferatien inhibition rate. DNA fragmentation gel analysis was used to analyze the cell apeptosis. DNA ploidy cell percentage were examined by flow cytometry（FCM）. The expression of VEGF was also examined by SP Immunohistochemistry and Western blot analysis. Results NS-398 in hibited HepG2 cells proliferration and induced apoptosis in a concentrationdependent manner. DNA ploidy analysis showed that S phase cell were significantly decerased and quiescent G1 phase was accumulated with NS-398 concentration increasing. The IC50 of 24 hours was 300 μmol/L. There was significant difference between the expression of VEGF in 200 、300 、400 μmol/L NS-398 groups and control groups. Conclusion NS-398 can inhibit the proliferation and induce apoptosis in HepG2 cells. The mechanism may be related with the accumulation of quiescent G1 phase and the inhibition of VEGF activity.

关 键 词：氮-2 环己氧-4 硝基苯-甲基磺胺 肝癌细胞 血管内皮生长因子 

分 类 号：R735.7[医药卫生—肿瘤]