中文摘要：

目的探讨染料异黄酮（genistein，GEN）和大豆苷元（daidzein，DAI）对人前列腺癌DU一145细胞凋亡的影响及其与过氧化物酶体增殖物激活体受体y（peroxisomeproliferators·activatedreceptor＇／，PPA脚）的关系。方法采用过氧化物酶体增殖物反应元件（peroxisomeproliferatorresponsiveelement，PPRE）驱动的荧光素酶报告基因检测GEN、DAI对DU，145细胞PPARl的激活作用；GEN、DAI单独或联合PPARy选择性拮抗剂GW9662处理Du一145细胞，采用免疫荧光化学染色方法观察PPAR~／定位分布变化；TUNEL法和AnnexinV／PI双染色流式细胞术检测细胞凋亡的变化。结果GEN、DAI明显增强转染PPRE．TK．Luc质粒的DU一145细胞中荧光素酶表达活性，且这种作用可被GW9662所逆转。GEN或DAI单独作用于DU．145细胞时，PPAR~发生核移位；细胞凋亡率明显增加（P〈0．05）。GW9662分别与GEN或DAI联合作用时，GEN、DAI促进PPAR吖核移位和诱导细胞凋亡的作用明显削弱（P〈0．05）。结论大豆异黄酮可通过激活PPAR~／信号途径，促进人前列腺癌DU一145细胞凋亡。

英文摘要：

Objective To investigate the effect of genistein （GEN） and daidzein （DAI） on apoptosis in human prostate cancer DU-145 cells and their correlation with peroxisome proliferators-activated receptor ~/ （PPAR~/）. Methods PPAR~/activity in prostate cancer DU-145 cells treated with soy isoflavones was mea- sured by peroxisome proliferator responsive element （PPRE）-driven luciferase reporter gene assay. DU-145 cells were respectively treated genistein and daidzein alone and either of them combined with GW9662, which was a selective inhibitor of PPAR~/, for 48 h. The expression and distribution of PPAR~/ were detected by immunofluorescence staining. Cell apoptosis was determined by TUNEL assay and Annexin V/P! dual-color flow cytometry. Results Genistein and daidzein significantly enhanced luciferase expression activity in DU-145 cells transfected with PPRE-TK-Luc plasmid, and the effect could be reversed by GW9662. The changes of PPAR~/expression in DU-145 ceils were not significant after treatment with either genistein or daidzein, but PPAR~/translocation to nucleus increased. The apoptotic rate of DU-145 cells treated with genistein or daidzein increased significantly （P 〈 0.05 ）. When cells were treated with either genistein or daidzein combined with GW9662, the increased apoptosis rate and PPAR~/nucleus translocation were significantly inhibited. Conclu- sion Soy isoflavones promote apoptosis in human prostate cancer DU-145 cells through PPAR7 activation.