Caffeic Acid,a Phenol Found in White Wine,Modulates Endothelial Nitric Oxide Production and Protects from Oxidative Stress-Associated Endothelial Cell Injury |
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| Authors: | Massimiliano Migliori Vincenzo Cantaluppi Claudio Mannari Alberto A E Bertelli Davide Medica Alessandro Domenico Quercia Victor Navarro Alessia Scatena Luca Giovannini Luigi Biancone Vincenzo Panichi |
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| Institution: | 1. Nephrology and Dialysis Unit, Versilia Hospital, Lido di Camaiore, Italy.; 2. Nephrology, Dialysis and Kidney Transplantation Unit, Department of Medical Sciences, University of Torino, Torino, Italy.; 3. Department of Translational Research and New Technology in Medicine, University of Pisa, Pisa, Italy.; 4. Department of Biomedical Sciences for Health, University of Milan, Milan, Italy.; University of Missouri, UNITED STATES, |
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| Abstract: | IntroductionSeveral studies demonstrated that endothelium dependent vasodilatation is impaired in cardiovascular and chronic kidney diseases because of oxidant stress-induced nitric oxide availability reduction. The Mediterranean diet, which is characterized by food containing phenols, was correlated with a reduced incidence of cardiovascular diseases and delayed progression toward end stage chronic renal failure. Previous studies demonstrated that both red and white wine exert cardioprotective effects. In particular, wine contains Caffeic acid (CAF), an active component with known antioxidant activities.Aim of the studyThe aim of the present study was to investigate the protective effect of low doses of CAF on oxidative stress-induced endothelial injury.ResultsCAF increased basal as well as acetylcholine—induced NO release by a mechanism independent from eNOS expression and phosphorylation. In addition, low doses of CAF (100 nM and 1 μM) increased proliferation and angiogenesis and inhibited leukocyte adhesion and endothelial cell apoptosis induced by hypoxia or by the uremic toxins ADMA, p-cresyl sulfate and indoxyl sulfate. The biological effects exerted by CAF on endothelial cells may be at least in part ascribed to modulation of NO release and by decreased ROS production. In an experimental model of kidney ischemia-reperfusion injury in mice, CAF significantly decreased tubular cell apoptosis, intraluminal cast deposition and leukocyte infiltration.ConclusionThe results of the present study suggest that CAF, at very low dosages similar to those observed after moderate white wine consumption, may exert a protective effect on endothelial cell function by modulating NO release independently from eNOS expression and phosphorylation. CAF-induced NO modulation may limit cardiovascular and kidney disease progression associated with oxidative stress-mediated endothelial injury. |
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