神经节苷脂GM3诱导U266细胞凋亡及作用机制研究

Apoptosis Effects of GM3 Ganglioside on U266 Cells and Its Possible Mechanism

目的:探讨神经节苷脂GM3对人多发性骨髓瘤U266细胞增殖抑制和诱导凋亡的作用及其可能的作用机制。方法:MTT法和流式细胞术检测不同浓度GM3作用U266细胞48 h后细胞增殖抑制及凋亡水平;实时荧光定量PCR检测不同浓度GM3对BCL-2、BAX mRNA表达水平的影响。结果:神经节苷脂GM3可以诱导U266细胞凋亡并抑制其增殖,且随着GM3浓度增加作用增强(早期凋亡率相关系数r=0.765,P<0.05;细胞增殖抑制率相关系数r=0.899,P<0.05);与对照组比较,实验组随着GM3浓度增加,凋亡基因BAX mRNA相对表达量逐渐升高(r=0.968,P<0.05),而抗凋亡基因BCL-2 mRNA相对表达量逐渐降低(r=-0.727,P<0.05)。结论:GM3可诱导U266细胞凋亡并抑制其增殖,且具有浓度依赖性。

Objective： To investigate the proliferation-inhibitory and apoptosis-inducing effect of ganglioside GM3 on human multiple myeloma cell line U266 cells and its possible mechanisms. Methods： MTT assay and flow cytometry were used to observe the effects of GM3 ganglioside on proliferation and apoptosis of human myeloma cell line U266.Effects of different concentration of ganglioside GM3 on the mRNA expression level of BCL-2 and BAX were detected by Real-time PCR. Results： MTT assay and Flow Cytometry showed that ganglioside GM3 could induce the apoptosis and inhibit the proliferation of multiple myeloma U266 cell line,and both the effects were enhanced with the increase of GM3 ganglioside concentration. Compared with the control group,the relative expression of BAX mRNA with the increase of GM3 concentration in experimental group was enhanced gradually（ r = 0. 968）,while the relative mRNA expression of anti-apoptotic gene BCL-2 was decreased gradually（ r =-0. 727）. Conclusion： GM3 ganglioside can induce apoptosis and inhibit the proliferation of U266 cell line in a concentration dependent manner. The mechanism may be related with up-regulation of BAX expression and down-regulation of BCL-2.