实用肝脏病杂志2016，Vol.19Issue(6)：704-708,5.DOI:10.3969/j.issn.1672-5069.2016.06.016
胰岛素抵抗肝癌细胞IGF-1R/NF-资B表达及多药耐药机制研究
Expression of IGF-1R/NF-kappa B and multi-drug resistance in insulin resistance-HepG2 and HepG2. 2.15 cells in vitro
摘要
Abstract
Objective To investigate the expression of insulin-like growth factor 1 receptor (IGF-1R), nuclear factor-κB (NF-κB) and the mechanism of multi-drug resistance (MDR) in insulin resistance (IR)-hepatoma cells in vitro. Methods The human hepatoma cells (HepG2 and HepG2.2.15) were induced by high concentration of insulin to establish a insulin resistance model. The expression of insulin receptor (InsR),IGF-1R,NF kappa B,P glycoprotein (P-gp) were detected by Western bloting and the effect of adriamycin on cell apoptosis were detected by flow cytometry (annexin V-FITC). Results IR model of hepatoma cells were established successfully by subjecting the HepG2 and HepG2.2.15 cells to 100 nmol/L and 1 000 n mol/L insulin respectively for 48 hours. The expression of IGF-1R,NF-kappa B and P-gp were up-regulated in IR hepatoma cells,while the InsR expression was down-regulated;After treatment of the two cells with 25 μg/ml doxorubicin for 24 hours,the apoptosis rate of IR-HpeG 2 cells (31.1% ±1.9%) was significantly lower than HepG2 cells [(49.7±2.2)%,P<0.01],and the apoptosis rate of IR-HepG2.2.15 cells (20.1±1.7)% was significantly lower than HepG2.2.15 cells [(33.8±1.8)%,P<0.01];The apoptotic rates of HepG2.2.15 or IR-HepG2.2.15 cells were significantly lower than HepG2 or IR-HepG2 cells(P<0.01),respectively. Conclusion The expression of IGF-1R, NF-kappa B and P-gp are up-regulated in IR-hepatoma cells,which might induce the MDR to adriamycin.关键词
HepG2细胞/胰岛素抵抗/胰岛素样生长因子1受体/核因子-κB/P 糖蛋白/多药耐药Key words
HepG2 cells/Insulin resistance/Insulin -like growth factor I receptor/NF-kappa B/P -glycoprotein/Multi-drug resistance引用本文复制引用
王以浪,印滇,杨莉,张亮,姚登福..胰岛素抵抗肝癌细胞IGF-1R/NF-资B表达及多药耐药机制研究[J].实用肝脏病杂志,2016,19(6):704-708,5.基金项目
南通市卫生局青年医学人才科研基金项目 （）
