Several 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.
The aim of the present study was to investigate the
protective effect of low doses of CAF on oxidative
stress-induced endothelial injury.
CAF 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.
The 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.
For more information
Migliori M, Cantaluppi V, Mannari C, Bertelli AAE,
Medica D, Quercia AD, et al. (2015) Caffeic Acid, a
Phenol Found in White Wine, Modulates Endothelial
Nitric Oxide Production and Protects from Oxidative
Stress-Associated Endothelial Cell Injury. PLoS ONE
10(4): e0117530.
doi:10.1371/journal.pone.0117530
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