土大黄苷对人乳腺癌细胞SK-BR-3凋亡的影响

摘要

目的:观察土大黄苷对人乳腺癌细胞SK-BR-3凋亡的影响.方法:Annexin V-FITC/PI双标法检测100、200、400 μmol/L土大黄苷对SK-BR-3细胞凋亡的影响,Western blot法检测Bcl-2及Bax蛋白的表达情况,试剂盒检测caspase-3的活性变化.结果:土大黄苷可诱导SK-BR-3细胞出现明显的早期凋亡,并呈浓度依赖性(P<0.05～P<0.01).土大黄苷在100、200、400 μmol/L浓度时均可抑制Bcl-2蛋白的表达,且随着其浓度的增加,蛋白表达逐渐降低,并促进Bax蛋白的表达(P<0.01).土大黄苷对caspase-3具有激活作用,且随着土大黄苷浓度的增加,caspase-3的活化程度逐渐增强.结论:土大黄苷具有诱导乳腺癌细胞凋亡的作用,其机制可能与调节凋亡相关蛋白Bcl-2、Bax的表达及激活caspase-3有关(P<0.01).%Objective: To investigate the effect of rhaponticin on apoptosis in human breast cancer SK-BR-3 cells. Methods: SK-BR-3 cells were treated with rhaponticin at the concentrations of 100,200,and 400 ?mol/L. Apoptosis was examined with Annexin V-FITC Apoptosis Detection Kit by flow cytometry. The expressions of Bcl-2 and Bax protein were analyzed by Western blot, caspase-3 activity was detected by special kit. Results: Rhaponticin induced obvious early apoptosis in SK-BR-3 cells in a concentration-dependent manner( P < 0. 05 to P < 0. 01) . Western blot results showed that rhaponticin enhanced the expression of Bax protein, and inhibited the expression of Bcl-2 protein, which was gradually down-regulated following the increase of rhaponticin's concentration ( P < 0. 01 ). Meanwhile, rhaponticin induced the activation of caspase-3 , and caspase-3 activity was increased with its concentration ( P < 0. 01 ) . Conclusions: Rhaponticin can induce apoptosis in SK-BR-3 cells, which may be correlated to the down-regulation of Bcl-2, the up-regulation of Bax, and the activation of caspase-3.