Limits...
Caffeic acid, a phenol found in white wine, modulates endothelial nitric oxide production and protects from oxidative stress-associated endothelial cell injury.

Migliori M, Cantaluppi V, Mannari C, Bertelli AA, Medica D, Quercia AD, Navarro V, Scatena A, Giovannini L, Biancone L, Panichi V - PLoS ONE (2015)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Nephrology and Dialysis Unit, Versilia Hospital, Lido di Camaiore, Italy.

ABSTRACT

Introduction: 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.

Aim of the study: The aim of the present study was to investigate the protective effect of low doses of CAF on oxidative stress-induced endothelial injury.

Results: 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.

Conclusion: 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.

Show MeSH

Related in: MedlinePlus

CAF increased NO production by HUVECs cultured in hypoxia or with uremic toxins.Representative fluorescence micrographs (A) and FACS analysis (B) of DAF-2DA probe on HUVECs cultured in hypoxia or with uremic toxins in presence or absence of CAF 1 μM. For immunofluorescence studies, magnification was x400; for FACS analysis, Kolmogorov-Smirnov statistical analysis was performed. For all assays, 5 independent experiments were performed with similar results.
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4390339&req=5

pone.0117530.g006: CAF increased NO production by HUVECs cultured in hypoxia or with uremic toxins.Representative fluorescence micrographs (A) and FACS analysis (B) of DAF-2DA probe on HUVECs cultured in hypoxia or with uremic toxins in presence or absence of CAF 1 μM. For immunofluorescence studies, magnification was x400; for FACS analysis, Kolmogorov-Smirnov statistical analysis was performed. For all assays, 5 independent experiments were performed with similar results.

Mentions: Hypoxia or the uremic toxins ADMA, p-cresyl sulfate and indoxyl sulfate reduced NO release from HUVECs as shown by immunofluorescence studies (Fig. 6A) and FACS analysis (Fig. 6B) using the DAF-2 DA probe. By contrast, CAF 1μM restored NO release from HUVECs cultured in hypoxia or with uremic toxins (Fig. 6A-B).


Caffeic acid, a phenol found in white wine, modulates endothelial nitric oxide production and protects from oxidative stress-associated endothelial cell injury.

Migliori M, Cantaluppi V, Mannari C, Bertelli AA, Medica D, Quercia AD, Navarro V, Scatena A, Giovannini L, Biancone L, Panichi V - PLoS ONE (2015)

CAF increased NO production by HUVECs cultured in hypoxia or with uremic toxins.Representative fluorescence micrographs (A) and FACS analysis (B) of DAF-2DA probe on HUVECs cultured in hypoxia or with uremic toxins in presence or absence of CAF 1 μM. For immunofluorescence studies, magnification was x400; for FACS analysis, Kolmogorov-Smirnov statistical analysis was performed. For all assays, 5 independent experiments were performed with similar results.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4390339&req=5

pone.0117530.g006: CAF increased NO production by HUVECs cultured in hypoxia or with uremic toxins.Representative fluorescence micrographs (A) and FACS analysis (B) of DAF-2DA probe on HUVECs cultured in hypoxia or with uremic toxins in presence or absence of CAF 1 μM. For immunofluorescence studies, magnification was x400; for FACS analysis, Kolmogorov-Smirnov statistical analysis was performed. For all assays, 5 independent experiments were performed with similar results.
Mentions: Hypoxia or the uremic toxins ADMA, p-cresyl sulfate and indoxyl sulfate reduced NO release from HUVECs as shown by immunofluorescence studies (Fig. 6A) and FACS analysis (Fig. 6B) using the DAF-2 DA probe. By contrast, CAF 1μM restored NO release from HUVECs cultured in hypoxia or with uremic toxins (Fig. 6A-B).

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Nephrology and Dialysis Unit, Versilia Hospital, Lido di Camaiore, Italy.

ABSTRACT

Introduction: 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.

Aim of the study: The aim of the present study was to investigate the protective effect of low doses of CAF on oxidative stress-induced endothelial injury.

Results: 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.

Conclusion: 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.

Show MeSH
Related in: MedlinePlus