Effects of Caffeoylglycosides on Arachidonate Metabolism in Leukocytes

Kimura, Yoshiyuki; Okuda, Hiromichi; Nishibe, Sansei; Arichi, Shigeru

doi:10.1055/s-2006-962658

Cited by 128 publications

(105 citation statements)

References 9 publications

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“…TxA2 mobilizes Ca2+ from intracellular stores; this intracellular elevation of Ca2+ is likely the final mediator of platelet aggregation and ADP release. It was also demonstrated that even at low concentrations (10 -6 -10 -3 mol/l) resveratrol inhibited the formation of lipoxygenase product and TXB2 by rat peritoneal polymorphonuclear leukocytes, and suppressed ADP-induced platelet aggregation (51).…”

Section: Mechanisms Involved In the Antiaggregatory Effect Of Wine Phmentioning

confidence: 94%

Alcohol, Wine and Platelet Function

Ruf¹

2004

Biol. Res.

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Epidemiological studies have demonstrated an inverse correlation between moderate wine and alcohol consumption and morbidity and mortality from coronary heart disease. The protective effect has been associated with an increase in the plasma level of HDL cholesterol, as it is well recognized that plasma HDL is inversely correlated with CHD. In addition, it has become evident that blood platelets contribute to the rate of development of atherosclerosis and CHD through several mechanisms. In recent studies it has been shown that the level of HDL cholesterol can explain only 50 % of the protective effect of alcoholic beverages; the other 50 % may be partly related to a decrease in platelet activity. This anti-platelet activity of wine is explained by ethanol but also by the polyphenolic components with which red wines are richly endowed. Several studies carried out on humans and animals have shown that wine phenolics could exert their effects by reducing prostanoid synthesis from arachidonate. In addition, it has been suggested that wine phenolics could reduce platelet activity mediated by nitric oxide. Moreover, wine phenolics increase vitamin E levels while decreasing the oxidation of platelets submitted to oxidative stress. However, a rebound phenomenon of hyperaggregability is observed after an acute alcohol consumption which is not observed with wine consumption. This protection afforded by wine has been duplicated in animals with grape phenolics added to alcohol. The rebound phenomenon may explain ischemic strokes or sudden deaths known to occur after episodes of drunkenness. It appears that wine, and wine phenolics in particular, could have a more significant inhibitory effect on platelet aggregation and could explain, in part, the hypothesis that red wine is more protective against atherosclerosis and coronary heart disease.

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Section: Mechanisms Involved In the Antiaggregatory Effect Of Wine Phmentioning

confidence: 94%

Alcohol, Wine and Platelet Function

Ruf¹

2004

Biol. Res.

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“…There were several pioneering reports on resveratrol, including a study of resveratrol as an inhibitor of arachidonate metabolism via interactions with 5-lipoxygenase and cyclooxygenase (COX) pathways in leukocytes. 6) However, resveratrol attracted little interest until 1992, when it was postulated to explain some of the cardioprotective effects of red wine. 7) Since that time, many studies have shown that resveratrol can prevent or slow the progression of a variety of conditions, including cancers, cardiovascular diseases, and ischemic injuries, [8][9][10][11][12] as well as enhance stress resistance and extend lifespan.…”

Section: Introductionmentioning

confidence: 99%

Recent Advances in the Study on Resveratrol

Nakata

Takahashi

Inoue

2012

Biological & Pharmaceutical Bulletin

152

112

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Appropriate long-term drinking of red wine is associated with a reduced risk for lifestyle-related diseases such as cardiovascular disease and cancer, making resveratrol, a constituent of grapes and various other plants, an attractive compound to be studied. Historically, resveratrol has been identified as a phytoalexin, antioxidant, cyclooxygenase (COX) inhibitor, peroxisome proliferator-activated receptor (PPAR) activator, endothelial nitric oxide synthase (eNOS) inducer, silent mating type information regulation 2 homolog 1 (SIRT1) activator, and more. Despite scepticism concerning the biological availability of resveratrol, a growing body of in vivo evidence indicates that resveratrol has protective effects in several stress and disease models. Here, we provide a review of the studies on resveratrol, especially with respect to COX, PPAR, and eNOS activities, and discuss its potential for promoting human health.

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“…The polyphenolic phytoalexin resveratrol (3,5,4'-trihydroxytrans-stilbene) became well known as a substance present in grapes and wine, especially in red wine, with pronounced pharmacological effects such as inhibition of cyclooxygenase I, antioxidant and anti-inflammatory activity, 1 inhibition of platelet aggregation and coagulation, 2 modulation of arachidonic acid metabolism, 3 lipid metabolism 4 and inhibition of low density lipoprotein oxidation. 5 ± 7 Based on these properties, it was suggested that resveratrol is a protective agent against cardiovascular diseases and may be responsible for the socalled French paradox, 8,9 namely, the lower frequency of myocardial disease in the population of Southern France, in spite of an intake of fat and cholesterol in amounts constituting a risk factor for cardiovascular disease.…”

Section: Introductionmentioning

confidence: 99%

Resveratrol causes arrest in the S-phase prior to Fas-independent apoptosis in CEM-C7H2 acute leukemia cells

et al. 2000

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Resveratrol (3,5,4'-trihydroxy-trans-stilbene), in the concentration range of 20 mM and above, induced arrest in the Sphase and apoptosis in the T cell-derived T-ALL lymphocytic leukemia cell line CEM-C7H2 which is deficient in functional p53 and p16. Expression of transgenic p16/INK4A, which causes arrest in G0/G1, markedly reduced the percentage of apoptotic cells. Antagonist antibodies to Fas or FasL, or constitutive expression of crmA did not diminish the extent of resveratrol-induced apoptosis. Furthermore, a caspase-8-negative, Fas-resistant Jurkat cell line was sensitive to resveratrol-induced apoptosis which could be strongly inhibited in the Jurkat as well as in the CEM cell line by z-VAD-fmk and z-IETD-fmk. The almost complete inhibition by z-IETD-fmk and the lack of inhibition by crmA suggested caspase-6 to be the essential initiator caspase. Western blots revealed the massive conversion of procaspase-6 to its active form, while caspase-3 and caspase-2 were proteolytically activated to a much lesser extent. Cell Death and Differentiation (2000) 7, 834 ± 842.

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Effects of Caffeoylglycosides on Arachidonate Metabolism in Leukocytes

Cited by 128 publications

References 9 publications

Alcohol, Wine and Platelet Function

Alcohol, Wine and Platelet Function

Recent Advances in the Study on Resveratrol

Resveratrol causes arrest in the S-phase prior to Fas-independent apoptosis in CEM-C7H2 acute leukemia cells

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