The role of polyphenolic compounds in the diet as inhibitors of platelet function

Abstract

Platelets play a substantial role in cardiovascular disease, and for many years there has been a search for dietary components that are able to inhibit platelet function and therefore decrease the risk of cardiovascular disease. Platelets can be inhibited by alcohol, dietary fats and some antioxidants, including a group of compounds, the polyphenols, found in fruits and vegetables. A number of these compounds have been shown to inhibit platelet function both in vitro and in vivo. In the present study the effects of the hydroxycinnamates and the flavonoid quercetin on platelet activation and cell signalling in vitro were investigated. The hydroxycinnamates inhibited platelet function, although not at levels that can be achieved in human plasma by dietary intervention. However, quercetin inhibited platelet aggregation at levels lower than those previously reported. Quercetin was also found to inhibit intracellular Ca mobilisation and whole-cell tyrosine protein phosphorylation in platelets, which are both processes essential for platelet activation. The effect of polyphenols on platelet aggregation in vivo was also investigated. Twenty subjects followed a low-polyphenol diet for 3 d before and also during supplementation. All subjects were supplemented with a polyphenol-rich meal every lunchtime for 5 d. Platelet aggregation and plasma flavonols were measured at baseline and after 5 d of dietary supplementation. Total plasma flavonoids increased significantly after the dietary intervention period (P=0·001). However, no significant changes in ex vivo platelet aggregation were observed. Further investigation of the effects of individual polyphenolic compounds on platelet function, both in vitro and in vivo, is required in order to elucidate their role in the relationship between diet and the risk of cardiovascular disease.

Antiplatelet Effects of Caffeic Acid Due to Ca2＋ MobilizationInhibition Via cAMP-Dependent Inositol-1, 4, 5-Trisphosphate Receptor Phosphorylation

“…3A) did not result from the degradanist to platelets, the value of IC50 (775 μM) of CAFA obtained in our human experiment is not significantly high compared with that (478.1±1.19 μM) obtained in another previous report 33) , because the degree of platelet aggregation is dependent on the dose of the agonist 34,35) . However, there appears to be a dose difference between humans and rats with respect to the antiplatelet effects of CAFA.…”

“…It has also been reported that a high value of IC50 (478.1±1.19 μM) of CAFA is required to inhibit collagen (1.0 μg/ mL)-induced human platelet aggregation in vitro 33) . Considering that the dose of collagen (10 μg/mL) used in our human experiment is 10-fold higher than that (1.0 μg/mL) used by Hubbard et al 33) as an agoplatelet aggregation, CAFA could be clinically applied to the prevention of platelet aggregation-mediated thrombosis, which means that CAFA may inhibit the human platelet-collagen interaction in the first step of collagen adhesion to the subendothelium of injured blood vessels. Therefore, we investigated whether CAFA inhibits collagen-induced human platelet aggregation.…”

Hydrophilic antioxidants of virgin olive oil. Part 1: Hydrophilic phenols: A key factor for virgin olive oil quality

“…In addition, both oleuropein and hydroxytyrosol inhibited vascular cell adhesion molecule-1 (VCAM-1) and reduced the stimulated expression of E-selectin and intercellular adhesion molecule-1 (ICAM-1), those three (CVAM-1, ICAM-1 and E-selectin) are thought to play a pivotal role in monocyte recruitment [106]. Besides, it was reported that flavonoids may contribute to prevention of cardiovascular diseases as luteolin was demonstrated to be a strong scavenger [33], and quercetin inhibits platelet aggregation both in vitro [107] and ex vivo [108,109], although its activity in vivo has yet to be confirmed.…”

Role of quercetin in cardiovascular diseases

“…Accumulated evidence has shown that reactive oxygen species are also the important mediators of cell signaling events such as inflammatory reactions (superoxides) and the maintenance of vascular tone (nitric oxide).However the overproduction of ROS such as superoxide has been associated with the pathogenesis of variety of diseases including cardiovascular diseases, diabetes, cancers, Alzheimer's disease, retinal degeneration, ischemic dementia and other neurodegenerative disorders and ageing 7,8,9 . Large numbers of studies have been conducted so far, showing the contributive role of quercetin to prevent cardiovascular diseases [10][11][12][13][14] . This article will review the process of oxidative stress mediated atherogenesis and their signaling pathway through which they relate to the cardiovascular diseases.…”