115. Anti-aggregating activity of trans- and cis-resveratrol

Bertelli, A. A. E.; Giovannini, Luca; Giannessi, D.; Panichi, Veronica; Bertelli, A.

doi:10.1016/s0268-9499(96)80692-8

Cited by 28 publications

(38 citation statements)

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“…A recent elegant`population study' now provides evidence that beverage intake of RSVL results in su¤-cient absorption/plasma levels to account for its bene¢cial health e¡ects [44]. Collectively, the present study suggests the MAPK and PTK pathways are important`targets' for the pathophysiological impact of ET-1 in the etiology of coronary heart diseases as well as for the putative cardiovascular protective e¡ects of RSVL.…”

Section: Discussionmentioning

confidence: 59%

Resveratrol inhibits MAPK activity and nuclear translocation in coronary artery smooth muscle: reversal of endothelin‐1 stimulatory effects

1999

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In porcine coronary arteries, short-term treatment with resveratrol (RSVL) substantially inhibited MAPK activity (IC 50 = 37 W WM); and immunoblot analyses revealed consistent reduction in the phosphorylation of ERK-1/-2, JNK-1 and p38, at active sites. Endothelin-1 (ET-1), a primary antecedent in coronary heart diseases, enhanced MAPK activity, phosphorylation and nuclear translocation in a concentration-responsive but RSVL-sensitive manner. RSVL had no effect on basal or forskolin-stimulated cAMP levels, a known downregulator of the MAPK cascade. Likewise, inhibition of MAPK by RSVL was not reversed by the estrogen receptor blockers tamoxifen and ICI-182,780. Conversely, RSVL remarkably attenuated basal and ET-1-evoked protein tyrosine phosphorylation. Because MAPKs promote smooth muscle proliferation and contraction, their current inhibition may contribute to the putative protection by RSVL against coronary heart diseases. These effects apparently do not involve interaction with estrogen receptors.z 1999 Federation of European Biochemical Societies.

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Section: Discussionmentioning

confidence: 59%

Resveratrol inhibits MAPK activity and nuclear translocation in coronary artery smooth muscle: reversal of endothelin‐1 stimulatory effects

1999

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“…Resveratrol, in a relatively high concentration [59,60], was reported to elicit vasodilation both in large conduit arteries and in vessels of the microcirculation in animal models (Fig. 3A) [61][62][63][64][65][66].…”

Section: Anti-oxidant Effects Of Resveratrolmentioning

confidence: 99%

Vascular Dysfunction in Aging: Potential Effects of Resveratrol, an Anti- Inflammatory Phytoestrogen

Labinskyy¹,

Csiszár²,

Veress³

et al. 2006

CMC

132

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Epidemiological studies demonstrated that even in the absence of other risk factors (e.g. diabetes, hypertension, hyperhomocysteinemia, hypercholesterolemia), advanced age itself significantly increases cardiovascular morbidity by enhancing vascular oxidative stress and inflammation. Because the population in the Western world is rapidly aging, there is a substantial need for pharmacological interventions that delay the functional decline of the cardiovascular system. Resveratrol is an atoxic phytoestrogen found in more than 70 plants including grapevine and berries. Recent data suggest that nutritional intake of resveratrol and other polyphenol compounds may contribute to the "French paradox", the unexpectedly low cardiovascular morbidity in the Mediterranean population. There is increasing evidence that resveratrol exerts multifaceted antioxidant and/or anti-inflammatory effects in various disease models. Importantly, resveratrol was reported to slow aging and increase lifespan in simple organisms and has been suggested as a potential calorie restriction mimetic. Resveratrol has also been reported to activate NAD-dependent histone deacetylases (sirtuins), which may contribute to its anti-aging effects. This review focuses on the role of oxidative stress and inflammation in cardiovascular dysfunction in aging, and on emerging anti-aging therapeutic strategies offered by resveratrol and other polyphenol compounds.

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“…Studies in male rats demonstrated that an alcohol-free red wine extract and resveratrol protect the heart from ischemia reperfusion injury (4). Rodent studies showed that orally administered resveratrol is absorbed in the gut, has high affinity for heart and liver (5,6), and is metabolized to glucuronides that have a t1 ⁄2 of ϳ1.5 h (7). A recurrent question is whether resveratrol, at concentrations present in red wine, is effective in vivo.…”

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confidence: 99%

Resveratrol and Estradiol Rapidly Activate MAPK Signaling through Estrogen Receptors α and β in Endothelial Cells

Klinge

Blankenship

Risinger

et al. 2005

Journal of Biological Chemistry

276

204

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Vascular endothelial cells (EC)are an important target of estrogen action through both the classical genomic (i.e. nuclear-initiated) activities of estrogen receptors ␣ and ␤ (ER␣ and ER␤) and the rapid "nongenomic" (i.e. membrane-initiated) activation of ER that stimulates intracellular phosphorylation pathways. We tested the hypothesis that the red wine polyphenol trans-resveratrol activates MAPK signaling via rapid ER activation in bovine aortic EC, human umbilical vein EC, and human microvascular EC. We report that bovine aortic EC, human umbilical vein EC, and human microvascular EC express ER␣ and ER␤. We demonstrate that resveratrol and estradiol (E 2 ) rapidly activated MAPK in a MEK-1, Src, matrix metalloproteinase, and epidermal growth factor receptor-dependent manner. Importantly, resveratrol activated MAPK and endothelial nitric-oxide synthase (eNOS) at nM concentrations (i.e. an order of magnitude less than that required for ER genomic activity) and concentrations possibly achieved transiently in serum following oral red wine consumption. Co-treatment with ER antagonists ICI 182,780 or 4-hydroxytamoxifen blocked resveratrol-or E 2 -induced MAPK and eNOS activation, indicating ER dependence. We demonstrate for the first time that ER␣-and ER␤-selective agonists propylpyrazole triol and diarylpropionitrile, respectively, stimulate MAPK and eNOS activity. A red but not a white wine extract also activated MAPK, and activity was directly correlated with the resveratrol concentration. These data suggest that ER may play a role in the rapid effects of resveratrol in EC and that some of the atheroprotective effects of resveratrol may be mediated through rapid activation of ER signaling in EC.Epidemiological studies have indicated that the consumption of red wine reduces the incidence of mortality from coronary heart disease (CHD) 1 (1, 2). The cardioprotective effect has been attributed to the polyphenol fraction of red wine (1). A key polyphenol in red wine is resveratrol, trans-3,5,4Ј-trihydroxystilbene, from grape skin. Red wine contains 1-75 mg of transresveratrol/liter (3). Studies in male rats demonstrated that an alcohol-free red wine extract and resveratrol protect the heart from ischemia reperfusion injury (4). Rodent studies showed that orally administered resveratrol is absorbed in the gut, has high affinity for heart and liver (5, 6), and is metabolized to glucuronides that have a t1 ⁄2 of ϳ1.5 h (7). A recurrent question is whether resveratrol, at concentrations present in red wine, is effective in vivo. The oral absorption of 25 mg of trans-

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115. Anti-aggregating activity of trans- and cis-resveratrol

Cited by 28 publications

References 0 publications

Resveratrol inhibits MAPK activity and nuclear translocation in coronary artery smooth muscle: reversal of endothelin‐1 stimulatory effects

Resveratrol inhibits MAPK activity and nuclear translocation in coronary artery smooth muscle: reversal of endothelin‐1 stimulatory effects

Vascular Dysfunction in Aging: Potential Effects of Resveratrol, an Anti- Inflammatory Phytoestrogen

Resveratrol and Estradiol Rapidly Activate MAPK Signaling through Estrogen Receptors α and β in Endothelial Cells

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