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A review of the mechanisms and effectiveness of dietary polyphenols in reducing oxidative stress and thrombotic risk
Author(s) -
Santhakumar A. B.,
Bulmer A. C.,
Singh I.
Publication year - 2014
Publication title -
journal of human nutrition and dietetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.951
H-Index - 70
eISSN - 1365-277X
pISSN - 0952-3871
DOI - 10.1111/jhn.12177
Subject(s) - medicine , oxidative stress , platelet , pharmacology , platelet activation , thromboxane a2 , reactive oxygen species , thromboxane , antioxidant , biochemistry , chemistry
Dietary sources of polyphenols, which are derivatives and/or isomers of flavones, isoflavones, flavonols, catechins and phenolic acids, possess antioxidant properties and therefore might be important in preventing oxidative‐stress‐induced platelet activation and attenuating adverse haemostatic function. Free radicals, including reactive oxygen and nitrogen species, promote oxidative stress, leading to platelet hyperactivation and the risk of thrombosis. The consumption of antioxidant/polyphenol rich foods might therefore impart anti‐thrombotic and cardiovascular protective effects via their inhibition of platelet hyperactivation or aggregation. Most commonly‐used anti‐platelet drugs such as aspirin block the cyclooxygenase (COX)‐1 pathway of platelet activation, similar to the action of antioxidants with respect to neutralising hydrogen peroxide (H 2 O 2 ), with a similar effect on thromboxane production via the COX ‐1 pathway. Polyphenols also target various additional platelet activation pathways (e.g. by blocking platelet‐ ADP , collagen receptors); thus alleviating fibrinogen binding to platelet surface ( GPII b‐ III a) receptors, reducing further platelet recruitment for aggregation and inhibiting platelet degranulation. As a result of the ability of polyphenols to target additional pathways of platelet activation, they may have the potential to substitute or complement currently used anti‐platelet drugs in sedentary, obese, pre‐diabetic or diabetic populations who can be resistant or sensitive to pharmacological anti‐platelet therapy.