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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-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γ(peroxisome proliferators-activated receptorγ,PPARγ)的关系。方法采用过氧化物酶体增殖物反应元件(peroxisome proliferator responsive element,PPRE)驱动的荧光素酶报告基因检测GEN、DAI对DU-145细胞PPARγ的激活作用;GEN、DAI单独或联合PPARγ选择性拮抗剂GW9662处理DU-145细胞,采用免疫荧光化学染色方法观察PPARγ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-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,PPARγ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PPARγ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PPARγ信号途径,促进人前列腺癌DU-145细胞凋亡。
Objective To investigate the effects of genistein (GEN) and daidzein (DAI) on the apoptosis of human prostate cancer DU-145 cells and its relationship with peroxisome proliferators- activated receptor gamma, PPAR gamma). METHODS: Peroxisome proliferator-responsive element (PPRE) -activated luciferase reporter gene was used to detect the activation of GEN and DAI on PPARγ in DU-145 cells. GEN and DAI selectively antagonized PPARγ alone or in combination with PPARγ. The change of localization of PPARγ was observed by immunofluorescent staining with agent GW9662. The apoptosis of DU-145 cells was detected by TUNEL and AnnexinⅤ / PI double staining. Results GEN and DAI significantly enhanced luciferase expression in DU-145 cells transfected with PPRE-TK-Luc plasmid, and this effect was reversed by GW9662. When GEN or DAI were treated alone, the nuclear translocation of PPARγ was observed; the apoptosis rate was significantly increased (P <0.05). GW9662 and GEN or DAI respectively, the effect of GEN and DAI on PPARγ nuclear translocation and apoptosis induction was significantly weakened (P <0.05). Conclusion Soy isoflavones can promote the apoptosis of human prostate cancer DU-145 cells by activating PPARγ signaling pathway.