Experimental and clinical studies support the pivotal role played by reactive oxidant species in the mechanism of platelet activation. This effect is achieved via multiple pathways, including enhanced formation of isoprostanes. Platelet NADPH oxidase seems to be the main source of platelet reactive oxidant species and isoprostanes. Pharmacologic approach that reduces platelet isoprostane formation may represent a future target of antiplatelet drugs. At this regard polyphenols would be of potential interest in virtue of their antioxidant property but interventional trials are necessary to see if they actually inhibit platelet aggregation in vivo and eventually prevent atherosclerotic progression.
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