Summary Resveratrol has been reported to have antiplatelet activity; however, the detailed mechanisms have not yet been resolved. This study aimed to systematically examine the detailed mechanisms of resveratrol in the prevention of platelet activation in vitro and in vivo. Resveratrol (0·05–0·25 μmol/l) showed stronger inhibition of platelet aggregation stimulated by collagen (1 μg/ml) than other agonists. Resveratrol (0·15 and 0·25 μmol/l) inhibited collagen‐induced platelet activation accompanied by [Ca+2]i mobilization, thromboxane A2 (TxA2) formation, phosphoinositide breakdown, and protein kinase C (PKC) activation. Resveratrol markedly increased levels of NO/cyclic guanosine monophosphate (GMP), and cyclic GMP‐induced vasodilator‐stimulated phosphoprotein phosphorylation. Resveratrol markedly inhibited p38 mitogen‐activated protein kinase (MAPK) but not Jun N‐terminal kinase or extracellular signal‐regulated kinase‐2 phosphorylation in washed platelets. Resveratrol‐reduced hydroxyl radical (OH−) formation in the electron spin resonance study. In an in vivo study, resveratrol (5 mg/kg) significantly prolonged platelet plug formation of mice. In conclusion, the main findings of this study suggest that the inhibitory effects of resveratrol possibly involve (i) inhibition of the p38 MAPK‐cytosolic phospholipase A2‐arachidonic acid‐TxA2‐[Ca+2]i cascade and (ii) activation of NO/cyclic GMP, resulting in inhibition of phospholipase C and/or PKC activation. Resveratrol is likely to exert significant protective effects in thromboembolic‐related disorders by inhibiting platelet aggregation.

[1] Although elastic velocities (V p , V s ) can be used to assess the distribution and concentration of marine gas hydrates in situ and several existing models relate hydrate saturation to acoustic velocity, the accuracy of these models is uncertain because of the difficulty in determining hydrate saturations and velocities of intact hydrate-bearing sediments. In this paper, the acoustic properties of gas hydrate-bearing consolidated sediments were investigated experimentally. Hydrate saturation (S h ) and acoustic velocities were measured in one system by time domain reflectometry and ultrasonic methods, respectively, during gas hydrate formation and subsequent dissociation in a water-saturated artificial core. Acoustic velocities change little at low hydrate saturations (0% to $10%), whereas they increase rapidly when hydrate saturation is between 10% and 30%. We verified two commonly used models, i.e., the weighted equation (WE) and the Biot-Gassmann theory modified by Lee (BGTL). In the 0% to 40% hydrate saturation range, the WE model is consistent with the measured V p data, while a combination of the WE and the V p /V s ratio in the BGTL predicts V s corresponding to the observed data. As hydrate saturation is more than 30%, however, the BGTL is more suitable for predicting both V p and V s . This suggests that gas hydrate may be treated as a component within a matrix of consolidated sediments when hydrate saturation exceeds 30%. However, when S h is less than 30%, the hydrate locates in the pore fluid or partly adheres to the sediment frame.

No abstract