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EnglishIntroduction: 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.
| Titolo: | Carotenoids Differentially Modulate Nitric Oxide Availability and Reduce TNF - Induced Monocyte-Endothelial Interaction |
| Autori: | |
| Data di pubblicazione: | 2010 |
| Rivista: | |
| 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. |
| Handle: | http://hdl.handle.net/11387/41530 |
| Appare nelle tipologie: | 1.5 Abstract in rivista |
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