中文摘要：

目的：探讨两种大豆异黄酮主要成分染料木黄酮（genistein,GEN）和大豆苷元（daidzein,DAI）抑制人乳腺癌MCF-7细胞增殖的作用与过氧化物酶体增殖激活物受体γ（peroxisome proliferators-activated receptorγ,PPARγ）信号途径的关系。方法：采用免疫细胞化学染色方法观察MCF-7细胞的PPARγ表达情况,PPARγ介导的荧光素酶报告基因检测大豆异黄酮和PPARγ配体罗格列酮（rosiglitazone,ROS）对MCF-7细胞PPARγ的激活作用,MCF-7细胞分别经8×10-5mol/L GEN、DAI和1×10-5mol/L的ROS单独或联合1×10-5mol/L的PPARγ特异性抑制剂GW9662联合处理24、48和72 h后,用CCK-8法检测细胞增殖。结果：MCF-7细胞存在有PPARγ表达,GEN、DAI呈剂量依赖性增强报告基因荧光素酶活性,且这种作用可被GW9662明显阻断;GEN、DAI和ROS呈时间依赖性明显抑制MCF-7细胞增殖（P〈0.05）,而GW9662可以显著削弱GEN、DAI和ROS对MCF-7细胞的增殖抑制作用（P〈0.05）。结论：大豆异黄酮可通过激活乳腺癌MCF-7细胞的PPARγ信号途径抑制其增殖。

英文摘要：

Objective：To investigate the effect of two major components of soy isoflavones genistein,daidzein and peroxisome on the proliferation of human breast cancer MCF-7 cells,and the relationship between it and the proliferators-activated receptor γ（PPARγ）signal pathway.Methods：The expression of PPARγ in breast cancer MCF-7 cells was detected by immunocytochemical staining,and the activation of PPARγ in MCF-7 cells induced by isoflavones was measured by luciferase reporter gene assay.The proliferation of MCF-7 cells was measured by CCK-8 assay.Results：There was expression of PPARγ in breast cancer MCF-7 cells.The luciferase ac-tivities of MCF-7 cells tranfected with luciferase reporter gene plasmid showed a dose-response relationship with genistein and daidzein treatment.GW9662 significantly inhibited the expression of reporter gene induced by genistein and daidzein.Genistein,daidzein and rosiglitazone inhibited the proliferation of cancer cells MCF-7in a time-dependent manner（P0.05）,but the inhibitory effects of genis-tein,daidzein and rosiglitazone on the proliferation of cancer cells could be blocked by GW9662 significantly（P0.05）.Conclusions：Soy isoflavones inhibit the proliferation of breast cancer MCF-7 cells by activating the PPARγ signal pathway.