异黄酮改构化合物F11对人乳腺癌细胞凋亡的影响及其机制研究  

Effect of an isoflavone derivative F11 on apoptosis of human breast cancer cells

作　　者：尹姝心[1] 艾国平[2] 常青[1] 杨伟[1] 粟永萍[2] 

机构地区：[1]第三军医大学西南医院妇产科,重庆400038 [2]第三军医大学军事预防医学院防原医学教研室,全军复合伤研究所,创伤、烧伤与复合伤国家重点实验室,重庆400038

出　　处：《第三军医大学学报》2009年第4期315-317,共3页Journal of Third Military Medical University

基　　金：重庆市科技攻关课题(2004BB5034);重庆市院士基金(2004BC5006)~~

摘　　要：目的研究异黄酮改构化合物F11对人乳腺癌细胞凋亡的影响及其机制。方法采用DNALadder、DAPI细胞核染色检测F11对人乳腺癌细胞MCF-7凋亡的影响,Westernblot检测凋亡相关蛋白Caspase-3、PARP、p53的表达。结果异黄酮改构化合物F11可诱导人乳腺癌细胞发生凋亡,增加Caspase-3和PARP蛋白的表达(P<0.01),抑制p53蛋白的表达(P<0.05,P<0.01)。结论异黄酮改构化合物F11诱导MCF-7发生凋亡,可能是通过诱导Caspase-3和PARP蛋白表达的增加,抑制p53蛋白的表达实现的。Objective To investigate the mechanism by which an isoflavone derivative F11 affects apoptosis of human breast cancer cell line MCF-7. Methods The apoptosis of MCF-7 cells induced by F11 was detected by DNA Ladder and DAPI dyeing. Western blot assay was used to detect the protein expressions of Caspase-3, PARP and p53. Results Fll induced cell apoptosis of MCF-7. After Fll treatment, the expressions of Caspase-3 and PARP increased, and the expression of mutant p53 decreased. Conclusion Isoflavone derivative F11 induces the apoptosis of breast cancer cells through upregulating the expressions of Caspase-3 and PARP, and decreasing p53 expression .

关 键 词：异黄酮改构化合物F11 MCF-7 凋亡 

分 类 号：R285.5[医药卫生—中药学] R730.23[医药卫生—中医学]