Key result
Hydroxytyrosol acetate demonstrated greater in vitro antiplatelet aggregating activity than hydroxytyrosol and similar activity to acetylsalicylic acid in human whole blood.
Why the study?
Does hydroxytyrosol acetate inhibit in vitro platelet aggregation in human whole blood compared to hydroxytyrosol and acetylsalicylic acid?
Does hydroxytyrosol acetate inhibit in vitro platelet aggregation in human whole blood compared to hydroxytyrosol and acetylsalicylic acid?
Hydroxytyrosol acetate, a polyphenol in virgin olive oil, demonstrates in vitro antiplatelet activity comparable to aspirin, suggesting a potential mechanism for the cardiovascular benefits of olive oil.
Supports further evaluation of hydroxytyrosol acetate for antiplatelet effects; leaves open clinical translation from in vitro data.
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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Correa et al. (2008) studied Healthy volunteers. Hydroxytyrosol acetate (HT-AC) vs. Hydroxytyrosol (HT) and acetylsalicylic acid (ASA) was evaluated on IC50 for inhibition of collagen-induced platelet aggregation in whole blood. Hydroxytyrosol acetate demonstrated greater in vitro antiplatelet aggregating activity than hydroxytyrosol and similar activity to acetylsalicylic acid in human whole blood.
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