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Virgin olive oil polyphenol hydroxytyrosol acetate inhibits in vitro platelet aggregation in human whole blood: comparison with hydroxytyrosol and acetylsalicylic acid.
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Virgin olive oil polyphenol hydroxytyrosol acetate inhibits in vitro platelet aggregation in human whole blood: comparison with hydroxytyrosol and acetylsalicylic acid.

Author: JA Correa Affiliation: Department of Pharmacology, Laboratorio de Investigaciones Antitrombóticas e Isquemia Tisular (LIAIT), School of Medicine, University of Málaga, Campus de Teatinos s/n, 29071 Málaga, Spain.JA López-VillodresR AsensiJL EsparteroG Rodríguez-GutiérezAll authors
Edition/Format: Article Article : English
Publication:The British journal of nutrition, 2009 Apr; 101(8): 1157-64
Other Databases: WorldCat
Summary:
Hydroxytyrosol acetate (HT-AC) is a polyphenol present in virgin olive oil (VOO) at a proportion similar to hydroxytyrosol (HT) (160-479 micromol/kg oil). The present study was designed to measure the in vitro platelet antiaggregating activity of HT-AC in human whole blood, and compare this effect with that of HT and acetylsalicylic acid (ASA). The experiments were designed according to the standard procedure to  Read more...
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Document Type: Article
All Authors / Contributors: JA Correa Affiliation: Department of Pharmacology, Laboratorio de Investigaciones Antitrombóticas e Isquemia Tisular (LIAIT), School of Medicine, University of Málaga, Campus de Teatinos s/n, 29071 Málaga, Spain.; JA López-Villodres; R Asensi; JL Espartero; G Rodríguez-Gutiérez; De La Cruz JP
ISSN:0007-1145
Language Note: English
Unique Identifier: 318652948
Awards:

Abstract:

Hydroxytyrosol acetate (HT-AC) is a polyphenol present in virgin olive oil (VOO) at a proportion similar to hydroxytyrosol (HT) (160-479 micromol/kg oil). The present study was designed to measure the in vitro platelet antiaggregating activity of HT-AC in human whole blood, and compare this effect with that of HT and acetylsalicylic acid (ASA). The experiments were designed according to the standard procedure to investigate the activity of ASA. HT-AC and HT inhibited platelet aggregation induced by ADP, collagen or arachidonic acid in both whole blood and platelet-rich plasma (PRP). ASA and HT-AC had a greater effect in whole blood than in PRP when ADP or collagen was used as inducer. ASA and HT-AC had a greater effect in PRP+leucocytes than in PRP alone. All three compounds inhibited platelet thromboxane B2 and leucocyte 6-keto-prostaglandin F1alpha (6-keto-PF1 alpha) production. The thromboxane/6-keto-PGF1alpha inhibition ratio (as an indirect index of the prostanoid equilibrium) was 10.8 (SE 1) for HT-AC, 1.0 (SE 0.1) for HT and 3.3 (SE 0.2) for ASA. All three compounds stimulated nitric oxide production, although HT was a weaker effect. In our experiments only concentrations higher than 500 microm (HT) or 1 mm (HT-AC and ASA) inhibited 3-nitrotyrosine production. All three compounds inhibited the production of TNFalpha by leucocytes, with no significant differences between them. In quantitative terms HT-AC showed a greater antiplatelet aggregating activity than HT and a similar activity to that of ASA. This effect involved a decrease in platelet thromboxane synthesis and an increase in leucocyte nitric oxide production.

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