芍药苷对人胃癌SGC7901/VCR细胞增殖抑制作用及其机制研究

Effect of paeoniflorin on apoptosis of human gastric cancer SGC7901 /VCR cells and its mechanism

目的:探索芍药苷(paeoniflorin)对人胃癌SGC7901/VCR细胞增殖抑制及凋亡的影响,并研究其可能的分子机制。方法:应用不同浓度芍药苷作用SGC7901/VCR细胞48h后,采用四甲基偶氮唑蓝法(MTT)检测细胞增殖抑制率;流式细胞术(FCM)检测细胞凋亡率;免疫蛋白印迹技术(Western blot)分析Bcl-2、Bax及细胞核内NF-κBp65蛋白的表达;酶联免疫吸附试验(ELISA)进一步确定核内NF-κB的转录活性。结果:芍药苷对SGC7901/VCR细胞生长有明显的抑制作用并促进其凋亡,这种作用呈现剂量依赖性;Westernblot和ELISA均证实芍药苷对NF-κB有明确抑制作用;随着芍药苷浓度增加NF-κB和Bcl-2表达水平逐渐下调(P<0.01),但对Bax没有明显影响。结论:芍药苷可明显抑制SGC7901/VCR细胞的增殖,诱导其凋亡;其机制部分可能与阻断NF-κB通路所介导的Bcl-2分子上调有关。

Objective：To explore the anti-tumor mechanism of paeoniflorin by human gastric cancer cell line SGC7901 /VCR.Methods：After SGC7901 /VCR cells were treated with paeoniflorin in different concentration for 48 h,methyl thaizolyl tetrazolium（MTT） method was used to detect the inhibition rates of the cells.Flow cytometry（FCM） was employed to detect SGC7901 /VCR cell apoptosis ratios.Western blot was used to test the expression of NF-κB,Bcl-2 and Bax.Activation of NF-κB transcription was detected by ELISA.Results：Paeoniflorin restrained cell proliferation and induced apoptosis of SGC7901/VCR cells in a dose-dependent manner.Paeoniflorin significantly inhibited the activity of NF-κB in nuclear.The inhibition pattern of NF-κB was confirmed by western blot and ELISA.After SGC7901 /VCR were treated with 0,40,80,160,320 μg /ml of paeoniflorin for 48 h respectively,the protein levels of Bcl-2 were down-regulated in a dose-dependent manner,while those of Bax were not affected.Conclusion：Paeoniflorin can inhibit the proliferation and induce the apoptosis of SGC7901 /VCR cells,which might be partly related to Bcl-2 up-regulation by inhibiting NF-κB activation.