Introduction: The activation of endothelium and subsequent enhanced monocytes adhesion and inflammatory response in blood vessels has been linked to cardiovascular disease. Nitric Oxide (NO) plays vascular anti-inflammatory action by inhibiting vascular adhesion molecules expression. Epidemiological studies suggest that carotenoid rich diets are associated with suppression and/or delay of cardiovascular disease progression, by a mechanism still partially known. We hypothesized that dietary carotenoids decrease vascular inflammatory response by increasing endothelial Nitric Oxide (NO) bioavailability. Methods and Materials: Human Umbilical Vein Endothelial Cells (HUVEC) was incubated with carotenoids (carotene [BC], lycopene [Lyc] and cryptoxanthin [Cry], 0.5-2.5 μmol/L) for 24 hours. HUVEC were then stimulated with Tumor Necrosis Factoralpha (TNF 1ng/mL) for 16 hours with subsequent determination of vascular cell adhesion molecules (VCAM-1), intercellular cell adhesion molecules (ICAM-1), E-Selectin protein levels. The functional consequences of HUVEC treatment with carotenoids on human monocytoid cell (U937 line) were also evaluated by adhesion assay. NF-kB pathway involvement and NO release were also evaluated. Results: BC and Lyc (1-2.5 mol/L) down regulated TNF induced NF B-dependent adhesion molecule expression and monocyte- HUVEC interaction. In parallel, BC and Lyc (2.5 mol/L) time-dependently increased NO bioavailability. TNF increased monocyte-HUVEC interaction, but not total adhesion molecules expression, NF-kB pathway activation and NO release, were inhibited by Cry. Conclusions: Our observations provide the evidence that all carotenoids studied inhibit. TNF increased monocytes adhesion to HUVEC. BC and Lyc exerted their anti-inflammatory action possibly by increasing NO bioavailability and this may contribute to explain why carotenoid rich diets are associated with reduced risk of cardiovascular disease.

Carotenoids Differentially Modulate Nitric Oxide Availability and Reduce TNF - Induced Monocyte-Endothelial Interaction

CIAVARDELLI, DOMENICO;
2010

Abstract

Introduction: The activation of endothelium and subsequent enhanced monocytes adhesion and inflammatory response in blood vessels has been linked to cardiovascular disease. Nitric Oxide (NO) plays vascular anti-inflammatory action by inhibiting vascular adhesion molecules expression. Epidemiological studies suggest that carotenoid rich diets are associated with suppression and/or delay of cardiovascular disease progression, by a mechanism still partially known. We hypothesized that dietary carotenoids decrease vascular inflammatory response by increasing endothelial Nitric Oxide (NO) bioavailability. Methods and Materials: Human Umbilical Vein Endothelial Cells (HUVEC) was incubated with carotenoids (carotene [BC], lycopene [Lyc] and cryptoxanthin [Cry], 0.5-2.5 μmol/L) for 24 hours. HUVEC were then stimulated with Tumor Necrosis Factoralpha (TNF 1ng/mL) for 16 hours with subsequent determination of vascular cell adhesion molecules (VCAM-1), intercellular cell adhesion molecules (ICAM-1), E-Selectin protein levels. The functional consequences of HUVEC treatment with carotenoids on human monocytoid cell (U937 line) were also evaluated by adhesion assay. NF-kB pathway involvement and NO release were also evaluated. Results: BC and Lyc (1-2.5 mol/L) down regulated TNF induced NF B-dependent adhesion molecule expression and monocyte- HUVEC interaction. In parallel, BC and Lyc (2.5 mol/L) time-dependently increased NO bioavailability. TNF increased monocyte-HUVEC interaction, but not total adhesion molecules expression, NF-kB pathway activation and NO release, were inhibited by Cry. Conclusions: Our observations provide the evidence that all carotenoids studied inhibit. TNF increased monocytes adhesion to HUVEC. BC and Lyc exerted their anti-inflammatory action possibly by increasing NO bioavailability and this may contribute to explain why carotenoid rich diets are associated with reduced risk of cardiovascular disease.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11387/41530
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