Scope: Cardiovascular disease (CVD) is associated with vascular oxidative imbalance and inflammation. Increased reactive oxygen species (ROS) generation is associated with a functional inactivation of nitric oxide (NO) due to the reaction with O₂⁻, leading to peroxynitrite (ONOO⁻) formation and subsequent reduction in the beneficial effect of vascular NO bioavailability. Carotenoids'-rich diets have been associated with decreased risk of CVD, but the underlying mechanism is still unknown.
Methods and results: In human umbilical vein endothelial cells (HUVECs), both β-carotene (BC) or lycopene (Lyc) significantly affected tumor necrosis factor-α (TNF-α)-induced inflammation, being associated with a significant decrease in the generation of ROS (spectrofluorometry) and nitrotyrosine (an index of ONOO⁻ formation, cytofluorimetry), an increased NO/cGMP (cyclic guanosine monophosphate) levels (EIA), and a down-regulation of NF-κB-dependent adhesion molecule expression (Western blot and EMSA) and monocyte-HUVEC interaction (adhesion assay). Our results indicate that BC or Lyc treatment reduce the inflammatory response in TNF-α-treated HUVECs. This is due to the redox balance protection and to the maintenance of NO bioavailability.
Conclusion: Our observations provide background for a novel mechanism for carotenoids' anti-inflammatory activity in the vasculature and may contribute to a better understanding of the protective effects of carotenoid-rich diets against CVD risk.
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