[ABSTRACT]Objective:To study the mechanism of Astragaloside II combined with 5-fluorouracil in inhibiting liver cell proliferation and to analyze the specific molecular mechanisms.Methods:Liver cancer cell lines HepG2 were cultured,cells of logphase growth were collected and treated with different conditions,blank control group were treated with DMEM without se-rum,5-Fu treatment group were treated with 0.5,1,5 and 10 μmol/L 5-Fu,and 5-Fu combined with Astragaloside II treat-ment group were treated with 10 μmol/L 5-Fu combined with 20,40 and 80 μmol/L Astragaloside II.24,48 and 72h after treatment,MTS kit was used to determine the cell viability;24h after treatment,Elisa kit was used to determine the content of apoptosis protein in cells.Results:Compared with blank control group,5-Fu treatment could reduce the survival rate of liver cancer cells in time-dependent and dose-dependent manner;compared with 10 μmol/L 5-Fu single drug treatment group,10μmol/L 5-Fu combined with Astragaloside II treatment could reduce the survival rate of liver cancer cells in time-dependent and dose-dependent manner;Fas,FasL,Bax,Caspase-3,Caspase-8 and Caspase-9 expression levels after 10 μmol/L 5-Fu treat-ment were significantly higher than those of blank control group,and Fas,FasL,Bax,Caspase-3,Caspase-8 and Caspase-9 expression levels after 10 μmol/L 5-Fu combined with 40 μmol/L Astragaloside II treatment were significantly higher than those of 10μmol/L 5-Fu treatment group.Conclusion:Astragaloside II combined with 5-fluorouracil treatment can enhance the inhibitory effect of 5-fluorouracil on liver cancer cell proliferation through mediating apoptosis proteins of Fas/FasL and Bax.%目的：：研究黄芪皂苷Ⅱ联合5-氟尿嘧啶处理对肝癌细胞增殖的影响并分析具体的分子机制.方法：培养肝癌细胞株 HepG2,取对数期生长的细胞并用不同条件进行处理,空白对照组用不含血清的DMEM 进行处理,5-Fu 处理组用0．5、1、5、10μmol/L 5-Fu 处理,5-Fu 联合黄芪皂苷 II 处理组用10μmol/L 5-Fu 联合20、40、80μmol/L 黄芪皂苷 II 处理.处理后24、48、72 h 时,采用 MTS 试剂盒测定细胞活力；处理后24 h 时,采用 Elisa 试剂盒测定细胞内凋亡蛋白的含量.结果：与空白对照组比较,5-Fu 处理能够以时间依赖性和剂量依赖性的方式降低肝癌细胞存活率；与10μmol/L 5-Fu 单药处理组比较,10μmol/L 5-Fu 联合黄芪皂苷 II 处理能够以时间依赖性和剂量依赖性的方式降低肝癌细胞存活率；10μmol/L 5-Fu 处理后的 Fas、FasL、Bax、Caspase-3、Caspase-8、Caspase-9表达量显著高于空白对照组,10μmol/L 5-Fu 联合40μmol/L 黄芪皂苷 II 处理后的 Fas、FasL、Bax、Caspase-3、Caspase-8、Caspase-9表达量显著高于10μmol/L 5-Fu 处理组.结论：黄芪皂苷 II 联合5-氟尿嘧啶处理能够增强5-氟尿嘧啶对肝癌细胞增殖的抑制效果,介导该作用的凋亡蛋白是 Fas/FasL 及 Bax.
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