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Endothelial cells deconjugate resveratrol metabolites to free resveratrol: a possible role in tissue factor modulation.

SCOPE: The antithrombotic effects of resveratrol (RV) and its derivatives remain unknown. The objective is to evaluate the modulatory effects of RV, its glucoside form, piceid, and its biological metabolites (RV-3-O-β-D-Glucuronide,RV-4'-O-D-Glucuronide,and RV-3-O-Sulfate) on tissue factor (TF). Moreover, the endothelial metabolism of RV is assessed.

METHODS AND RESULTS: Human aortic endothelial cells (HAECs) were incubated with trans-piceid, trans-RV or their biological metabolites and stimulated with tumour necrosis factor-α (TNF-α). TF activity, protein levels, and mRNA expression were determined in cell lysates. Moreover, RV conjugation (phase-II-metabolism) to its sulfated or glucuronidated metabolites and their deconjugation to their parent compound (free RV) were also assessed in cell lysates and culture media. RV decreased TF activity, protein levels, and mRNA expression, whereas piceid and RV metabolites (RVmet) had no effects. RV-3-O-Sulfate was the main metabolite generated in the endothelium, while RVmet were deconjugated to free RV. Isomerization of trans-RV and its trans-metabolites to their cis-forms, was observed.

CONCLUSIONS: RV exerts antithrombotic effects by modulating TF. RVmet and piceid did not exert this effect. However, the capacity of endothelial cells to deconjugate RVmet to free RV indicates that RVmet function as an endothelial reservoir for RV regeneration, thus contributing to the antithrombotic effects of RV. This article is protected by copyright. All rights reserved.

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