摘要
目的探讨选择性环氧合酶-2抑制剂NS-398对人肝癌HepG2细胞株的生长抑制、诱导凋亡及其对bcl-2表达的影响。方法采用MTT法检测细胞增殖,流式细胞术检测细胞周期、凋亡及凋亡相关蛋白bcl-2的表达。结果NS-398抑制HepG2的增殖活性,经20、40、80和160μmol/L的NS-398处理细胞48h后,其抑制率分别为6.72%、16.21%、20.86%和25.34%,呈剂量依赖效应关系;细胞经160μmol/L的NS-398处理24h、48h和72h后,G0/G1期细胞由76.07±0.75%分别减少至62.27±0.74%、59.17±1.47%和53.03±1.60%(P<0.05),S期细胞由11.40±0.79%分别增加至13.23±0.81%、16.20±1.95%和16.60±1.25%(P<0.05),G2/M期细胞无明显变化;凋亡细胞增多,凋亡率分别为8.47%、16.3%和23.9%;细胞经160μmol/L的NS-398处理48h后bcl-2蛋白与对照组比,表达下调(P<0.01)。结论NS-398对人肝癌细胞株HepG2有抑制增殖、诱导凋亡作用,细胞凋亡的机制可能与细胞凋亡相关基因bcl-2表达下调有关。
Objective To investigate the effects of NS-398,an cyclooxygenase-2 selective inhibitor,on the proliferation and apoptosis of HepG2 cells. Methods The proliferation of cells was detected by MTT assay. The cell cycle and apoptosis associated with bcl-2 were detected by flow cytometry. Results NS-398 inhibited the proliferation of human HepG2 cells at a dose-dependent manner. When interfered with NS-398 at a dose of 20,40,80 and 160μmol/L for 48h, the inhibiting rates were 6.72% ,16.21% ,20.86% and 25.34% ,respectively; and when interfered with 160μmol/L NS-398 for 24h,48h and 72h,the cells of G0/G1 from 76.07± 0.75% reduced to 62.27±0. 74%,59.17± 1.47% and 53.03± 1. 600/60 ,respectively（P 〈0.05） ; the cells of S stage from 11.40±0. 790/60 increased to 13.23±0.81% ,16.20±1. 950/60 and 16.60±1.25 %,respectively（P〈0.05）. The cell of G2/M stage was not markedly changed; The apoptotic cells increased with the apoptosis rates of 8.47 0/60,16.3 0/60 and 23.9 0/60, respectively. The expression of bcl-2 decreased obviously as compared with control group（P〈0. 01）. Conclusion NS-398 can inhibit the proliferation and induce apoptosis of HepG2,which might be related to the down regulated expression of bcl-2.
出处
《实用肝脏病杂志》
CAS
2008年第1期20-23,共4页
Journal of Practical Hepatology
