摘要
目的:观察华蟾素(cinobufacini)对白血病HL-60细胞的增殖抑制作用和诱导凋亡作用的机制。方法:以HL-60细胞为研究对象,采用MTT法观察细胞增殖作用;Annexin V-FITC/PI双染和吖啶橙/溴乙锭(AO/EB)荧光染色法检测细胞凋亡;罗丹明染色法检测线粒体膜电位;分光光度法检测Caspase-3活性。结果:在0.78～6.25μg·m^(-1),华蟾素能明显的抑制HL-60细胞的增殖;华蟾素作用24h后,Annexin V阳性的细胞从7.81%增加至66.02%,而且在荧光显微镜下可以明显观察到凋亡细胞;线粒体膜电位下降和Caspase-3活性升高。结论:华蟾素能够抑制HL-60细胞增殖,这种作用与其诱导细胞凋亡破坏线粒体功能和激活Caspase-3有关。
Objective： To investigate the effects of proliferation inhibitory and the molecule mechanism of apoptosis induced by cinobufacini on HL-60 cells. Method： Human leukenfia HL-60 cells were used. The effects of cinobufacini on cell proliferation were ohserved by MTT method in vitro. The apoptods was evaluated by Annexin V-FITC/PI and AO/EB fluorescent staining. Mitochondfial membrane potential and Caspase-3 were measured. Result： Cinobafacini exhibited a marked antiproliferative effect on HL-60 cells within the concentration from 0.78 to 6.25μg·ml^-1. Annexin V positive cells increased from 7.81% to 66.02% and apoptotie cells were observed under fluorescence microscope. Mitochondrial membrane potential was dissipated and caspase-3 activity was increased （P〈 0.05）. Collclusion： Cinobufacini can inhibit the proliferation on HL-60 cell effectively. The effect may be correlated with apoptosisinducing activity. Cinobufacini-indueed apoptosis appear to involve the dissipation mitochondrial membrane potential.
出处
《中国药师》
CAS
2008年第10期1158-1160,共3页
China Pharmacist
