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β‐Carotene and lycopene affect endothelial response to TNF‐α reducing nitro‐oxidative stress and interaction with monocytes
Author(s) -
Di Tomo Pamela,
Canali Raffaella,
Ciavardelli Domenico,
Di Silvestre Sara,
De Marco Alessandro,
Giardinelli Annalisa,
Pipino Caterina,
Di Pietro Natalia,
Virgili Fabio,
Pandolfi Assunta
Publication year - 2012
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201100500
Subject(s) - oxidative stress , chemistry , nitric oxide , peroxynitrite , reactive oxygen species , umbilical vein , inflammation , nitrotyrosine , tumor necrosis factor alpha , pharmacology , biochemistry , reactive nitrogen species , peroxynitrous acid , lycopene , sulforaphane , superoxide , carotenoid , nitric oxide synthase , immunology , biology , in vitro , organic chemistry , enzyme
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 O − 2 , 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.