A systematic review of the biological effects of resveratrol on venous thromboembolism

TL;DR

This paper reviews how resveratrol may help prevent and treat venous thromboembolism by reducing inflammation, oxidation, and blood clotting.

Contribution

A systematic review of resveratrol's biological mechanisms in preventing venous thromboembolism, highlighting antioxidant, anti-inflammatory, and anticoagulant effects.

Findings

Resveratrol inhibits reactive oxygen species and proinflammatory pathways like NF-κB in venous thromboembolism.

Resveratrol regulates coagulation and reduces adhesion molecules, promoting endothelial protection and vasodilation.

In vitro and in vivo studies show resveratrol's potential against deep vein thrombosis and pulmonary embolism.

Abstract

Venous thromboembolism (VTE) has high morbidity in major surgery, serious injury, or during periods of inflammation and infection. VTE has serious complications, resulting in death. This review aims to evaluate the efficacy and mechanisms of resveratrol (RSV) in preventing and treating deep vein thrombosis (DVT) and pulmonary embolism (PE).

Various databases like MEDLINE/PubMed, Embase, Scopus, Cochrane Library, and Web of Science were comprehensively searched to find relevant studies published before January 2024. After defining the inclusion and exclusion criteria, selecting studies related to the purpose of the study, data were extracted, and study characteristics, methods, and biological mechanisms were recorded and reviewed.

RSV potentially prevents and attenuates VTE through antioxidant, anti-inflammatory, and anticoagulant mechanisms. It inhibited endothelial and platelet reactive oxygen species (ROS) production, enhanced endogenous antioxidants, and downregulated nuclear factor kappa B (NF-κB) and proinflammatory cytokines. RSV also regulated coagulation and fibrinolysis, inhibited tissue factor (TF) and myeloperoxidase (MPO), and reduced apoptosis. Additionally, RSV reduced adhesion molecule expression, including vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule 1 (ICAM-1), P-selectin, and von Willebrand Factor (vWF), while promoting vasodilation and endothelial protection through increased nitric oxide (NO) production, SIRT1 activation, and ANGPT2 expression.

In vivo and in vitro studies have revealed that RSV has promising effects on DVT and PE. However, more well-designed controlled clinical trials with human subjects are needed to examine its application in clinical settings.

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