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作 者:陈美霓[1] 郭巍[2] 赵菊梅[1] 魏晓丽[1] 王爱红[1] 庞秋霞[1]
机构地区:[1]延安大学医学院实验中心,陕西延安716000 [2]延安大学医学院附属医院泌尿外科,陕西延安716000
出 处:《中国医药导报》2014年第30期12-15,共4页China Medical Herald
基 金:陕西省教育厅科研计划项目(编号12JK0713);陕西省高水平大学建设专项资金资助项目(编号2013SXTS 02);陕西省延安市科学技术研究发展计划项目(编号2013-KW15)
摘 要:目的观察17-AAG对人肝癌HepG2细胞增殖和凋亡的影响并探讨其机制。方法四甲基偶氮唑蓝(MTT)比色法检测不同浓度的17-AAG对肝癌HepG2细胞增殖的影响;荧光显微镜观察碘化丙啶(PI)染色的细胞凋亡形态;流式细胞仪检测分析细胞周期分布和凋亡率的变化;免疫组化法检测肝癌HepG2细胞中重组人血管内皮生长因子相关蛋白(VEGF-C蛋白)表达水平变化。结果不同浓度的17-AAG呈时间、剂量依赖性抑制肝癌HepG2细胞的生长增殖(P<0.05);流式细胞仪分析显示,17-AAG作用HepG2细胞48 h后G2/M期细胞比例上升,G1/G0期细胞比例下降;0.63、1.25、2.5、5.0μmol/L 17-AAG作用HepG2细胞48 h后的凋亡率分别为(3.23±1.43)%、(9.71±2.20)%、(14.15±2.34)%、(23.65±2.58)%;随着药物浓度的加大,VEGF-C蛋白表达逐渐减少。结论 17-AAG对肝癌HepG2细胞有抑制增殖、诱导凋亡的作用,并能抑制VEGF-C蛋白的表达。Objective To study the effect of 17-allylamino-17-demethoxygelda-namycin(17-AAG) on cell proliferation and apoptosis in human hepatoma carcinoma cell lines HepG2 and analyze the possible mechanism. Methods The human hepatoma carcinoma cell lines HepG2 cells were treated with different concentrations of 17-AAG in vitro, the cell proliferation was analyzed by the MTT; the cell apoptosis changes was observed using PI dyeing under the fluorescence microscope; the effect of 17-AAG on apoptosis and cell cycle were assayed through flow cytometry; the expression of VEGF-C protein was detected by immunohistochemistry. Results 17-AAG significantly suppressed the proliferation of HepG2 cells in a time and dose-dependent manner(P 0.05). Flow cytometry analysis showed that 17-AAG could increase the cell population in G2/M phase and reduce the cell population in G1/G0 phase at 48 h. HepG2 cells were treated with 17-AAG of 0.63, 1.25, 2.5 and 5.0 μmol/L concentrations for 48 h, the apoptosis rate were(3.23±1.43)%,(9.71±2.20)%,(14.15±2.34)% and(23.65±2.58)%. The expression of VEGF-C protein was reduced with the increase of drug concentration. Conclusion 17-AAG can inhibit proliferation and induce apoptosis of HepG2 cells, and can decrease the expression of VEGF-C protein.
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