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作者机构:Univ Florence Dept Surg & Translat Med I-50139 Florence Italy Univ Florence DISIA Dept Stat PHYTOLAB I-50139 Florence Italy
出 版 物:《NUTRITION AND CANCER-AN INTERNATIONAL JOURNAL》 (营养与癌症)
年 卷 期:2014年第66卷第7期
页 面:1228-1236页
核心收录:
学科分类:12[管理学] 1204[管理学-公共管理] 120402[管理学-社会医学与卫生事业管理(可授管理学、医学学位)] 1004[医学-公共卫生与预防医学(可授医学、理学学位)] 1002[医学-临床医学] 10[医学]
基 金:F.I.R.M.O. Fondazione Raffaella Becagli
主 题:OLIVE RNA physiology THERAPEUTIC use of olive oil COLON tumors PREVENTION ACADEMIC medical centers BIOLOGICAL assay CELL culture CELL physiology NUTRITION PHENOLS PLANT extracts DATA analysis MICROARRAY technology DESCRIPTIVE statistics IN vitro studies THERAPEUTIC use
摘 要:The Mediterranean diet is associated with a lower incidence of atherosclerosis, cardiovascular diseases, and some types of cancer. Recent interest has been focused on the biological activity of phenolic compounds present in extra virgin olive oils (EVOOs). Both in vivo and in vitro studies have shown that EVOO components have positive effects on metabolic parameters, such as plasma lipoproteins, oxidative damage, inflammatory markers, platelet function, and antimicrobial activity. We have investigated the possible interactions between 2 extracts of extra virgin olive oil and estrogen receptor beta (ER beta) in an in vitro model of colon cancer. The qualification and quantification of the components of the 2 samples tested showed that phenolic compounds-hydroxytyrosol, secoiridoids, and lignans-are the major represented compounds. EVOO extracts were tested on a colon cancer cell line engineered to overexpress ER beta (HCT8-beta 8). By using custom made Oligo microarray, gene expression profiles of colon cancer cells challenged with EVOO-T extracts when compared with those of cells exposed to 17 beta-estradiol (17 beta-E2). This study demonstrated that the EVOO extracts tested showed an antiproliferative effect on colon cancer cells through the interaction with estrogen-dependent signals involved in tumor cell growth. Specifically, the ability of EVOO extracts to inhibit cell proliferation was superimposable to the activation of the ER beta receptor, similar to what was observed after 17 beta-E2 challenge.