九节龙皂苷诱导胶质瘤SHG-44细胞凋亡及其机制研究

目的研究九节龙皂苷对胶质瘤SHG-44细胞潜在的治疗作用及其机制。方法用四甲基偶氨唑蓝（MTT）法检测不同剂量九节龙皂苷于不同时间（6、12、24、72h）对人胶质瘤SHG-d4细胞活性的影响和细胞流式术检测SGH-44细胞调亡情况;Western—blot检测caspase-3和Bcl-2在SHG-44细胞中的表达情况。结果流式细胞仪检测显示,随着九节龙皂苷浓度的增大和时间延长,SHG-44细胞的凋亡率明显上升,Western—blot结果提示九节龙皂苷下调了凋亡抑制蛋白Bcl-2的表达并激活了凋亡蛋白caspase-3,九节龙皂苷明显抑制SHG-44细胞的生长与增殖。结论九节龙皂苷引起胶质瘤细胞大量凋亡,具有显著的抗肿瘤作用,通过调控caspase-3和Bcl-2诱导胶质瘤SHG-44细胞凋亡。

Apoptosis of glioma SHG-44 cells induced by ardipusilloside and its mechanism

Objective To study the potential therapeutic effect of saponin ardipusilloside on human glioma SHG-44 cells and the related mechanism of apoptosis. Methods Methyl thiazolyl tetrazolium （MTF） assay was performed to measure the effect on the proliferation of SHG-44 cells＇ treated by different concentrations of ardipusilloside for 6,12,24,72 hours. The apoptosis of SGH-44 cells was detected by flow cytometry. Western-blot revealed the expression of caspase-3 and Bcl-2 in SGH-44 cells. Results Ardipusilloside significantly inhibited the cell viability of SHG-44 cells in a concentration- and time-dependent manner and induced SHG-44 cells apoptosis. It is suggested that ardipusilloside could down-regulate the expression of anti-apoptosic protein Bcl-2 and activate the pro-apoptotic protein caspase. Conclusion Ardipusilloside could effectively induce the apoptosis of glioma SHG-44 cells which was due to the activation of caspase cascade and the inhibition of antiapoptotic protein Bcl-2.