研究薯蓣皂苷对HepG2肝癌细胞增殖的抑制作用。不同浓度薯蓣皂苷干预HepG2肝癌细胞24 h后，采用MTT法、Hoechst33258染色法、JC-1染色法和Western blot法检测细胞的增殖能力、线粒体膜电位水平、活性氧水平和Bax、Bcl-2表达。结果显示，2.00 μmol/L薯蓣皂苷组对HepG2细胞的抑制率为41.69%，高于1.00 μmol/L薯蓣皂苷组；薯蓣皂苷干预HepG2细胞后，细胞分布密度降低，出现变圆脱落死亡；升高ROS水平、降低MMP、抑制Bcl-2和上调Bax的表达，与对照组相比均有显著性差异。2.00 μmol/L薯蓣皂苷组Bcl-2、Bax相对表达量分别为0.08、0.10。以上实验结果表明，薯蓣皂苷可明显抑制HepG2肝癌细胞的增殖能力，诱导其发生凋亡，其机制可能与其通过线粒体途径降低MMP，抑制Bcl-2蛋白的表达，上调Bax蛋白的表达有关。
The inhibitory effects of dioscin on the proliferatino of HepG2 cells were investigated. HepG2 cells were first treated with dioscin at different concentrations for 24 h. The proliferation ability, mitochondrial membrane potentials (MMP), reactive oxide species, and the Bcl-2 and Bax expressions of cells were detected by MTT assay, Hoechst 33258 staining, JC-1 staining, and western blotting. Results show an inhibition rate of 41.69% on the HepG2 cells treated with dioscin at 2.00 μmol/L. This rate is higher than that noted for the group treated with 1.00 μmol/L dioscin. After dioscin treatment, the distribution density of HepG2 cells reduces, and the cells become rounded, detached, and dead. At the same time, the ROS level increases, whereas the MMP decreases. Furthermore, the Bcl-2 protein expression is inhibited and that of Bax is enhanced. The experimental groups show significant differences from the control group. The relative expression levels of Bcl-2 and Bax in the 2.00 μmol/L dioscin-treated group are 0.08 and 0.10, respectively. The aforementioned results indicate that dioscin can effectively inhibit the proliferation ability and induce the apoptosis of HepG2 cells. This may be realized given that dioscin can reduce the MMP through mitochondrial pathways. As such, dioscin can enhance the protein expression of Bax and inhibit that of Bcl-2.