黄芪多糖对肝癌HepG2细胞的抑制作用及其机制

被引:25
作者
冯涛 [1 ]
张保国 [2 ]
机构
[1] 南京市市级机关医院药剂科
[2] 南京医科大学附属南京第一医院肿瘤科
关键词
黄芪多糖; 肝癌HepG2细胞株; 细胞增殖; 细胞凋亡;
D O I
暂无
中图分类号
R735.7 [肝肿瘤];
学科分类号
摘要
目的研究黄芪多糖(APS)和5-氟尿嘧啶(5-fu)联合使用对肝癌HepG2细胞的生长抑制及其作用机制。方法用RPMI1640培养液对低分化人肝癌细胞株HepG2进行传代培养,取对数生长期细胞,分为5组:A组:对照组,不含药物,使用同体积的磷酸盐缓冲液(PBS);B组:APS组,只给予100μg/mlAPS;C组:5-fu组,只给予100μg/ml5-fu;D组:5-fu+低浓度APS组,给予100μg/ml5-fu+100μg/mlAPS;E组:5-fu+高浓度APS组,给予100μg/ml5-fu+200μg/mlAPS。用噻唑蓝(MTT)法观察APS及5-fu对HepG2细胞增殖的影响;用流式细胞术方法测药物作用后细胞周期变化和细胞凋亡;western-blot检测凋亡相关蛋白表达。结果 APS和5-fu联合使用可抑制HepG2细胞的增殖,效应呈浓度和时间依赖性;APS和5-fu联合使用阻滞HepG2细胞周期于G1期;并可诱导HepG2细胞凋亡;APS和5-fu联合使用,可明显增高肝癌HepG2细胞中caspase-3、caspase-9蛋白的表达,同时检测到抑凋亡蛋白Bcl-2表达显著降低。在只使用5-fu的实验组细胞中均未检测到上述变化。结论 APS和5-fu联合使用能抑制肝癌HepG2细胞株的增殖,其机制之一是影响细胞周期使之阻滞于G1期,激活了细胞凋亡系统,从而诱导细胞凋亡。
引用
收藏
页码:486 / 488+495 +495
页数:4
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