中文摘要：

目的研究环境雌激素辛基酚（OP）和三羟异黄酮（GEN）对大鼠乳腺癌中血管内皮生长因子（VEGF）及其受体（flk-1）和血小板源性因子受体-4（CxCR4）表达的影响。方法雌性SD大鼠随机分为对照组（Con）、模型组（Mod）及3个实验组：GEN、OP和GP（GEN＋OP）。二甲基苯蒽启动致乳腺癌（Con组除外），第210d处死大鼠，用免疫组化和免疫印迹检测大鼠乳腺及乳腺癌组织中VEGF、flk-1和CXCR4表达。结果与Mod组比较，GEN组VEGF、flk-1和CXCR4蛋白表达均降低，OP组VEGF、flk-1和CXCR4表达增高，GP组CXCR4降低。结论GEN通过下调乳腺癌组织中VEGF、flk-1和CXCR4的表达量，降低大鼠乳腺癌的发生，OP则通过上调VEGF、flk-1和CXCR4的嘉汰倬乳障癌的枯毕塞增加．

英文摘要：

Objective To study the effects of enviromental estrogen chemicals octylphenol（OP）and genistein（GEN） on the expressions of vascular endothelial growth factor（VEGF）, VEGF receptor（ilk-1） and CXC chemokine receptor type 4 （CXCR4） in rat breast cancer. Methods Female Sprague - Dawley rats were randomly divided into control, model, GEN treated, OP treated and GP（GEN ＋ OP） treated group. After 7, 12 - dinmethylbenz[a]anthracene（DMBA） induced rat breast cancers（Except rats in control group）, rats were killed on day 210. Western blotting and immunohistoehemistry methods were used to detect the expressions of VEGF, CXCR4 and ilk - 1 on normal mammary grand and mammary cancers. Results Compared with model group, VEGF, CXCR4 and ilk - 1 expressions were significantly decreased in mammary cancers of genistein treated group, while they were significantly increased in oetylphenol treated group. CXCR4 expression was significantly decreased in GP treated group. Conclusion GEN is down - regulate VEGF, CXCR4 and ilk - 1 expressions in mammary cancer then may inhibits the incidences of DMBA - induced mammary cancers. OP is up - regulate VEGF, CXCR4 and ilk- 1 expressions in mammary cancer then may increase the incidences of DMBA- induced mammary cancers.