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作 者:谢闺娥[1] 杜晶春[1] 徐霞[1] 董桂兰[2]
机构地区:[1]广州医科大学金域检验学院,广东广州510182 [2]广州大学门诊部,广东广州510006
出 处:《大连医科大学学报》2016年第3期215-218,共4页Journal of Dalian Medical University
基 金:国家自然科学基金项目(81101682);广东省公益研究与能力建设专项资金项目(2014A020212015)
摘 要:目的研究扁蒴藤素对乳腺癌细胞MCF-7生长和凋亡的影响及其机制。方法用MTT法检测扁蒴藤素对MCF-7细胞细胞生长的影响;用Annexin V-FITC/PI双染及TUNEL染色检测扁蒴藤素对MCF-7凋亡的诱导作用;用western blot分析扁蒴藤素作用后,凋亡相关因子Bcl-2和Bax蛋白的表达变化。结果扁蒴藤素对MCF-7细胞的生长有显著的抑制作用,对其作用48 h的半数抑制浓度(IC50)为0.59μmol/L。1.0μmol/L扁蒴藤素作用后,Annexin V-FITC/PI染色凋亡细胞比率(15.55±1.43)%,TUNEL阳性的MCF-7细胞比率为(35.59±4.43)%,较对照组(未经扁朔藤素作用)[(1.45±0.24)%和(0.85±0.34)%]明显升高,差异均有显著性意义,P<0.05。Western blot结果显示,扁蒴藤素能下调Bcl-2的表达,上调Bax的表达。结论扁蒴藤素素通过调节细胞凋亡相关因子诱导MCF-7细胞凋亡的发生,从而高效抑制MCF-7乳腺癌细胞的生长。Objective To investigate the effect of pristimerin on the growth and apoptosis of MCF-7 breast cancer cells and to explore the underlying mechanism. Methods The effect of pristimerin on the growth and of apoptosis MCF-7 cells were analyzed by MTT assay and Annexin V-FITC/PI staining,TUNEL staining,respectively. The expression of Bcl-2 and Bax was determined by western blotting analysis. Results Pristimerin exhibited a marked inhibition on the survival of MCF-7 cells,and the half maximal inhibitory concentration( IC50) value was 0. 59 μmol/L.The numbers of apoptotic MCF-7 cells,as revealed by Annexin V binding and TUNEL assay,increased upon pristimerin treatment. Pristimerin treatment resulted in a decrease of Bcl-2 and an increase of Bax expression. Conclusion Our results demonstrated that pristimerin suppressed the proliferation of MCF-7 cells,and that these effects occurred through increasing apoptosis by regulation of apoptotic effectors.
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