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作 者:赵素容[1] 刘浩[1] 梁颖[1] 钱江华[1] 陈超[1] 蒋志文[1]
机构地区:[1]蚌埠医学院药学系,安徽省生化药物工程技术研究中心,安徽蚌埠233030
出 处:《蚌埠医学院学报》2012年第7期845-847,共3页Journal of Bengbu Medical College
基 金:安徽省高校省级优秀青年人才基金资助项目(2010SQRL122);蚌埠医学院科研资助项目(BY0823)
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、400μmol/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、400μmol/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 μmoL/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 〈 O. O1 ). 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 ). Condusions:Rhaponticin can induce apoptosis in SK-BR-3 calls, which may be correlated to the clown-regulation of Bcl-2, the up- regulation of Bax, and the activation of caspase-3.
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