Evidence and Mechanisms of Resveratrol Against Platelet Function: A Literature Review and Network Pharmacology

Globally, cardiovascular disease stands as a leading cause of mortality, with platelets pivotal in the pathogenesis of thrombosis and atherosclerosis. Platelet function, including adhesion, activation, aggregation and apoptosis, is critical for hemostasis and thrombosis and is regulated by multiple mechanisms. The utilization of bioactive compounds derived from plants is being regarded as a promising approach for controlling the risk of atherosclerosis cardiovascular disease. Resveratrol (RES) is a polyphenol present in various plants, notably grapes and berries, exhibiting anti-inflammatory, antioxidant, and cardiovascular protective properties. Moreover, RES has been proven to inhibit platelet hyperreactivity in animals and in vitro. In this review, we summarize the anti-platelet mechanisms of RES, which include inhibiting agonist-mediated platelet activation, attenuating COX-1-mediated TXA2 release, enhancing antioxidant capacity, and modulating Sirt1-mediated signaling. We further summarize that the regulation of the gut microbiome and its metabolites, as well as the anti-inflammatory effects, are indirect mechanisms attributed to its low bioavailability. Additionally, we found that RES may exert regulatory effects on the platelet apoptosis via Network Pharmacology Exploration. In conclusion, current evidence suggests that RES demonstrates inhibitory effects on platelet function in vitro and animal models. However, there remains insufficient evidence from population-based studies to be explored.