Red wine polyphenols improve an established aging-related endothelial dysfunction in the mesenteric artery of middle-aged rats: Role of oxidative stress

2012 ◽  
Vol 419 (2) ◽  
pp. 381-387 ◽  
Author(s):  
Stéphanie Dal-Ros ◽  
Christian Bronner ◽  
Cyril Auger ◽  
Valérie B. Schini-Kerth
Keyword(s):  
Oxidative Stress ◽  
Endothelial Dysfunction ◽  
Mesenteric Artery ◽  
Red Wine ◽  
Aged Rats ◽  
Middle Aged ◽  
Wine Polyphenols ◽  
Red Wine Polyphenols

Endothelium-derived contracting factors mediate the Ang II-induced endothelial dysfunction in the rat aorta: preventive effect of red wine polyphenols

2009 ◽  
Vol 459 (5) ◽  
pp. 671-679 ◽  
Author(s):  
Modou O. Kane ◽  
Nelly Etienne-Selloum ◽  
Soccoro V. F. Madeira ◽  
Mamadou Sarr ◽  
Allison Walter ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Red Wine ◽  
Rat Aorta ◽  
Ang Ii ◽  
Preventive Effect ◽  
Wine Polyphenols ◽  
Red Wine Polyphenols

scholarly journals Proteomic analysis of Saccharomyces cerevisiae to study the effects of red wine polyphenols on oxidative stress

2019 ◽  
Vol 56 (9) ◽  
pp. 4129-4138
Author(s):  
Mariana S. Lingua ◽  
Ricardo M. Neme Tauil ◽  
Carlos Batthyány ◽  
Daniel A. Wunderlin ◽  
María V. Baroni
Keyword(s):  
Oxidative Stress ◽  
Saccharomyces Cerevisiae ◽  
Proteomic Analysis ◽  
Red Wine ◽  
Wine Polyphenols ◽  
Red Wine Polyphenols

Role of endothelial cell membrane transport in red wine polyphenols-induced coronary vasorelaxation: involvement of bilitranslocase

2013 ◽  
Vol 4 (10) ◽  
pp. 1452 ◽  
Author(s):  
Lovro Ziberna ◽  
Jong-Hun Kim ◽  
Cyril Auger ◽  
Sabina Passamonti ◽  
Valérie Schini-Kerth
Keyword(s):  
Endothelial Cell ◽  
Cell Membrane ◽  
Membrane Transport ◽  
Red Wine ◽  
Wine Polyphenols ◽  
Red Wine Polyphenols ◽  
Cell Membrane Transport

Red wine polyphenols prevent endothelial dysfunction induced by endothelin-1 in rat aorta: role of NADPH oxidase

2010 ◽  
Vol 120 (8) ◽  
pp. 321-333 ◽  
Author(s):  
Rocío López-Sepúlveda ◽  
Manuel Gómez-Guzmán ◽  
Maria José Zarzuelo ◽  
Miguel Romero ◽  
Manuel Sánchez ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Nadph Oxidase ◽  
Endothelial Function ◽  
Oxidase Activity ◽  
Red Wine ◽  
Vascular Wall ◽  
Nadph Oxidase Activity ◽  
Wine Polyphenols ◽  
Red Wine Polyphenols ◽  
O2 Production

RWPs (red wine polyphenols) exert antihypertensive effects and improve endothelial function by reducing the plasma levels of ET-1 (endothelin-1) and the subsequent vascular production of O2•− (superoxide anion). Our present study was designed to evaluate whether RWPs act directly in the vascular wall improving endothelial dysfunction and O2•− production induced by ET-1 and to analyse the compounds responsible for these protective effects. We incubated rat isolated aortic rings in the presence or absence of ET-1 (10 nM) and RWPs (10−4 to 10−2 g/l) or catechin (0.2 μM), epicatechin (10 μM) and resveratrol (0.1 μM). ET-1 reduced the relaxant responses to acetylcholine, increased intracellular O2•− production, NADPH oxidase activity and protein expression of NADPH oxidase subunit p47phox. All these changes were prevented by RWPs. The preventive effects of RWPs were unaffected by co-incubation with either ICI-182780, an ER (oestrogen receptor) antagonist, or GW9662, a PPARγ (peroxisome-proliferator-activated receptor γ) antagonist. RWPs inhibited the phosphorylation of the mitogen-activated protein kinase, ERK1/2 (extracellular signal-regulated kinase 1/2), a key regulator of p47phox expression in response to ET-1. When the isolated polyphenols were tested, at the concentrations found in 10−2 g/l RWPs, only epicatechin prevented endothelial dysfunction and all biochemical changes induced by ET-1 in the vascular wall. Taken together, these results indicate that RWPs prevent ET-1-induced vascular O2•− production by reducing overexpression of p47phox and the subsequent increased NADPH oxidase activity, leading to improvement in endothelial function. The effects of RWPs appear to be independent of ER and PPARγ activation and are related to ERK1/2 inhibition.

P2253Intake of the omega 3 PUFAs formulation EPA:DHA 6:1 by aged rats reduced shedding of microvesicles from spleen-derived cultured leukocytes and their ability to promote senescence in endothelial cells

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
A W Qureshi ◽  
R Altamimy ◽  
A El Habhab ◽  
L Amoura ◽  
S Khemais-Berkhiat ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
Inflammatory Responses ◽  
Premature Senescence ◽  
Aged Rats ◽  
Omega 3 ◽  
Middle Aged ◽  
Angiotensin System ◽  
Coronary Syndrome

Abstract Introduction Ageing is associated with the appearance of endothelial senescence promoting endothelial dysfunction and, ultimately, cardiovascular events. Circulating microvesicles (MVs) of patients with acute coronary syndrome promoted premature endothelial senescence by stimulating the local angiotensin system. Omega 3 PUFAs have been shown to reduce the risk of cardiovascular disease in patients at high risk. Purpose This study investigated whether a 7-day intake of the omega 3 formulation EPA:DHA 6:1 by rats affects the level of MVs released by spleen-derived cultured leukocytes as well as their ability to promote premature senescence in target endothelial cells (ECs), and, if so, to clarify the underlying mechanism. Methods Middle-aged male Wistar rats (M, 48-week old) received 500 mg/kg/d of either EPA:DHA 6:1, EPA:DHA 1:1, or vehicle (CTL) for 7 days. Thereafter, spleen-derived leukocytes, a rich source of MVs, were prepared and cultured for 24 h. Cultured ECs were prepared from porcine coronary arteries. Senescence-associated β-galactosidase activity (SA-β-gal) was assessed by C12FDG, protein expression level by Western blot analysis, oxidative stress by dihydroethidium using confocal microscopy, and procoagulant MVs by prothrombinase assay. Spleen-derived leukocytes from untreated young (Y, 12-week) and old (O, 72-week) rats were also studied. Results Shedding of MVs by spleen-derived leukocytes significantly increased with increasing age. Incubation of ECs with leukocyte-derived MVs (10 nM Phtd Ser eq.) from M and O but not those from Y induced premature senescence after 48 h. The stimulatory effect of M-MVs was prevented by losartan and associated with oxidative stress. M-MVs induced an upregulation of senescence markers (p16, p21, p53), pro-atherothrombotic markers (VCAM-1, ICAM-1, tissue factor), the pro-inflammatory marker cyclooxygenase-2 (COX-2) but not COX-1, and of the angiotensin system (angiotensin-converting enzyme and type 1 angiotensin receptor), whereas endothelial NO synthase was down-regulated. A one-week intake of EPA:DHA 1:1 and 6:1 by M rats decreased the leukocyte-derived MVs shedding by about 14% and 24%, and EPA:DHA 6:1 reduced their ability to induce ECs senescence by 38%. The stimulatory effect of M-MVs on the expression of target proteins was also observed with those from the EPA:DHA 1:1 but not with those from the 6:1 group. Conclusion These findings indicate that ingestion of EPA:DHA 6:1 by middle-aged rats reduces not only the shedding of MVs by spleen-derived leukocytes but also their ability to induce pro-senescent, pro-thrombotic and pro-inflammatory responses in endothelial cells most likely by decreasing the local angiotensin system. They further suggest that EPA:DHA 6:1 may help to delay ageing-related endothelial dysfunction. Acknowledgement/Funding Unrestricted research grant from PIVOTAL Therapeutics Inc.

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