摘要
目的通过将淫羊藿苷(ICA)联合丝裂霉素(MMC)联合作用肝癌HepG2细胞的实验研究,探讨联合药物对HepG2细胞增殖的抑制作用及其可能的机制。方法 MTT法检测不同浓度ICA、MMC或两药联合处理48 h后及未处理组HepG2细胞的增殖活性,通过两药相互作用系数CDI评价两种药物的相互作用性质;RT-PCR检测药物处理后HepG2细胞内凋亡抑制蛋白质FLIP mRNA水平的变化。结果单独ICA或MMC处理后,均可抑制HepG2细胞的增殖,其抑制率随着药物剂量增加而增强(P<0.05),呈剂量依赖性;两药联合应用对HepG2细胞增殖的抑制作用明显,其抑制率呈剂量依赖性(P<0.01),且两药作用具有协同效应(CDI<1);与未处理组相比,ICA或MMC处理后HepG2细胞内FLIP mRNA水平降低,尤其以联合药物处理组降低更加显著(P<0.001)。结论 ICA与MMC联用可在体外抑制肝癌细胞的增殖,两药具有协同效应,其抑制机制可能通过抑制凋亡抑制蛋白FLIP的表达,从而增加癌细胞的凋亡而实现的。
Purpose To investigate the anti-proliferative effect of icariin(ICA) combined with mitomycin C(MMC) on the HepG2 cells and its possible mechanism.Methods The inhibitory effect of ICA or MMC or in both on HepG2 cells was measured by MTT assay.The coefficient of drug interaction(CDI) was used to analyze the nature of these two drugs interactions.The FLIP mRNA levels were detected by RT-PCR.Results ICA or MMC had anti-proliferative effect on HepG2 cells in a dose-dependent manner.Co-inhibitory effects were observed after treatment with a combination of ICA(25,50 μg/mL) and MMC(2,4 μg/mL),and CDI were significant(CDI<1).The FLIP mRNA level decreased in drugtreated groups,especially in combination group.Conclusion ICA could enhance anti-proliferative effect of MMC on HepG2 cells at designated doses and the possible mechanism probably induced apoptosis via down-regulation apoptosis-inhibitory protein FLIP.
出处
《中国生化药物杂志》
CAS
CSCD
北大核心
2011年第1期22-25,共4页
Chinese Journal of Biochemical Pharmaceutics
