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作 者:康敏[1] 钟德君[1] 杜光红[1] 任美萍[1]
机构地区:[1]泸州医学院附属医院消化内科,四川泸州646000
出 处:《泸州医学院学报》2011年第1期44-47,共4页Journal of Luzhou Medical College
摘 要:目的:观察过氧化物酶体增殖物激活受体γ(PPARγ)的配体罗格列酮(RSG)对肝癌细胞增殖的影响。方法:体外培养人肝癌HepG2细胞,应用CCK-8比色法检测不同浓度RSG(25、50、100、200μmol/L)和不同作用时间RSG(24h、48h、72h)对肝癌HepG2细胞增殖的影响;流式细胞仪(FCM)检测细胞周期;实时荧光定量PCR方法分析细胞周期蛋白CyclinD1的mRNA表达变化;免疫细胞化学法分析CyclinD1的蛋白表达变化。结果:RSG抑制肝癌HepG2细胞增殖,CCK-8比色法显示增殖抑制率与RSG的浓度-时间呈正相关;FCM检测发现,RSG使肝癌HepG2细胞的细胞周期被阻滞于G1期,而进入S期的细胞明显减少,且呈浓度依赖;RSG干预后,CyclinD1的mRNA及蛋白表达在肝癌细胞中下调。结论:RSG依赖激活PPARγ途径能在体外抑制肝癌细胞生长,提示PPARγ可能是肝癌治疗的一个新分子靶点。Objective:To investigate of effect of rosiglitazone(RSG),the ligand of peroxisome proliferator activated receptor gamma(PPARγ),on proliferation of human hepatocarcinoma cell.Methods:Human hepatocarcinoma HepG2 cell line was cultured in vitro.The effect of RSG of different concentrations(25、50、100、200υmol·L-1)and different action times(24、48、72hours)on the growth of hepatocarcinoma cells HepG2 was detected by Cell Counting Kit-8(CCK-8) analysis.The change of cell cycle at each concentration were detected by flow cytometry(FCM).The expression of CyclinD1 mRNA and protein were investigated by real-time fluorescent quantitive polymerase chain reaction and immunocytochemical method respectively.Results:RSG showed significant effect on inhibiting the cell proliferation.CCK-8 assay indicated that RSG could inhibit the proliferation of HepG2 cells in a concentration time dependent manner.FCM showed the cell cycle of HepG2 cells was arrested at G1 stage by RSG in a concentration dependent manner real-time fluorescent quantitive polymerase chain reaction and immunohistochemical techniques indicated the down-regulation of CyclinD1 mRNA and protein expression.Conclusion:These results indicate that the growth-inhibitory effcet of RSG is mediated through PPARγ signaling pathway in hepatocarcinoma cell in vitro,suggesting that PPARγ might be a novel therapeutic target for hepatocarcinoma.
关 键 词:罗格列酮 过氧化物酶体增殖激活受体Γ 肝癌 增殖
分 类 号:R329.25[医药卫生—人体解剖和组织胚胎学]
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