索拉菲尼联合阿霉素对人肝癌细胞株HepG2的抑制作用

目的：探讨索拉非尼（Sorafenib）和阿霉素（adriamycin）联合用药对肝癌细胞株nepG2的作用及可能的机制。方法：以不同浓度索拉非尼和不同浓度阿霉素分别组成单药组和索拉非尼＋阿霉素联合用药组作用于HepG2细胞,MTT法检测增殖抑制率、流式细胞仪分析细胞周期和凋亡率。结果：索拉非尼、阿霉素单药与联用均能抑制HepG2细胞增殖,呈剂量依赖效应,两药联用有协同效应（P〈0.01）。索拉非尼、阿霉素单药与联用均能诱导HepG2细胞凋亡,并以联合组更为明显,与对照组比较有显著的统计学意义（P〈0.01）。索拉非尼及阿霉素单药作用均可使细胞周期阻滞于G0-G1期,联合用药组G0/Gl期细胞比率低于索拉非尼及阿霉素单药组,S期细胞比率高于单药组;阿霉素能抑制HepG2细胞Survivin mRNA表达诱导细胞的凋亡。结论：索拉非尼与阿霉素联合作用于人肝癌HepG2细胞具有协同作用,其机制可能是通过多途径共同抑制HepG2细胞增殖及诱导细胞凋亡。

Coadministration of Sorafenib with Adriamycin Inhibits Cell Proliferation in Hepatocellular Carcinoma Cells HepG2

Objective： To investigate the inhibitory effect of sorafenib in combination with adriamycin in human hepatocellular carcinoma cell line HepG2 in vitro and explore its possible mechanisms.Methods： HepG2 cells were treated with different concertration of sorafenib or adriamycin alone or their combination.The inhibitory effects were detected by MTT assay,and cycle arrest and apoptosis of HepG2 cells were analyzed by flow cytometry in different groups.Results： Sorafenib or adriamycin used in alone or combination in-hibited the proliferation of HepG2 cells.The inhibiting rates increased with the increasing concentrations of sorafenib or adriamycin alone or their combination,and a synergistic effects was observed in their combined action（P0.01）.The combination treatment resulted in significantly higher apoptosis than those in other groups（P0.01）.HepG2 cells cycle were blocked in G0-G1 period in Sorafenib or adriamycin alone or their combination.The combination treatment of the cells ratio in G0-G1 period were lower than those of Sorafenib or adriamycin used alone.The percentage of HepG2 cells in S period increased.Adriamycin down-regulate expression of survivin mRNA in HepG2 cells and inducing HepG2 cells apoptosis.Conclusions： A synergistic effect is observed between the sorafenib and adriamycin in their inhibition of HepG2 cell proliferation and inducing cell apoptosis,the mechanisms of which may involve synergistic effect of in-hibition with many pathway.