【摘要】 目的观察大黄素(Emodin,EM)对血小板衍生生长因子(platelet-derived growth factor,PDGF)诱导的人肝癌HepG2细胞体外增殖的影响并探讨其作用机制。方法体外培养HepG2细胞,经一定量的PDGF或PDGF与EM共同作用后,以MTT法检测细胞活力;流式细胞术检测细胞凋亡和细胞周期;免疫细胞化学法检测细胞NF-κB及PDGF的表达。结果在2.5~5.0ng/mL浓度范围内,外源性PDGF可明显促进HepG2细胞增殖,抑制细胞凋亡,影响细胞周期,使G0/G1期比例降低,S期比例增高。并能增强NF-κB的表达,PDGF各处理组与对照组相比,P<0.05。而EM可明显抑制PDGF的上述作用,EM处理组与PDGF处理组相比,细胞增殖数、细胞凋亡率、细胞周期分布、NF-κB的表达差异均有统计学意义,P<0.05。且EM可直接抑制PDGF的表达。结论EM对PDGF诱导的人肝癌HepG2细胞增殖有显著抑制效应,其机制可能与直接减弱PDGF的效应有关。更多还原

【Abstract】 OBJECTIVE:To investigate the effects of emodin on proliferation of human hepatoma cell HepG2 induced by PDGF in vitro, and to explore the underlying mechanism. METHODS: HepG2 cell were exposed to PDGF or PDGF combining emodin; the proliferative activity of cells was determined by MTT assay; the cell cycle and cell apoptosis analysis were evaluated by FCM; the effects of emodin on expression of NF-κB and PDGF were assessed by immunocytochemistry. RESULTS: In the concentration of 2.5-5.0 ng/mL, exogenous PDGF-A and PDGF-B significantly promoted the proliferation of HepG2 cells, inhibited apoptosis of the cells,with cell cycle shortened, cells of phrase G0/G1 reduced and cells of phrase S increased, and they also induced the expression of NF-κB. There were significants difference among the experiment groups and control group, P<0.05. However, emodin inhibited these effects of PDGFs on HepG2 cells. After the treatment of emodin, there were significant alterations in the proliferation of HepG2 cells, apoptosis rate, cell cycle distribution and the expression of NF-κB, P<0.05. Whats more, emodin inhibited the expression of PDGF directly. CONCLUTIONS: Emodin can markedly inhibit proliferation of HepG2 cells. The mechanism might be related to block the effects of PDGFs directly.更多还原