Abstract
Diabetes is associated with vascular inflammation, endothelial dysfunction, and oxidative stress, promoting the development of cardiovascular diseases (CVD). Several studies showed that a carotenoid-rich diet is associated to a reduced cardiovascular risk in healthy and diabetic subjects, although the mechanisms of action are still unknown. Here, the potential role of β-carotene (BC) and lycopene (Lyc) in human endothelial cells isolated from human umbilical cord vein (HUVECs) of women with gestational diabetes (GD) and respective controls (C) has been investigated. Results showed that BC and Lyc reduced the tumor necrosis factor alpha- (TNF-α-) stimulated monocyte-endothelium interaction (adhesion assay), membrane exposure (flow cytometry), and total expression levels (Western blot) of VCAM-1 and ICAM-1 in both cell types. Moreover, the treatment with BC and Lyc reduced the TNF-α-induced nuclear translocation of NF-κB (image flow cytometry) by preserving bioavailability of nitric oxide (NO, flow cytometry, and cGMP EIA kit assay), a key vasoactive molecule. Notably, BC and Lyc pretreatment significantly reduced peroxynitrite levels (flow cytometry), contributing to the redox balance protection. These results suggest a new mechanism of action of carotenoids which exert vascular protective action in diabetic condition, thus reinforcing the importance of a carotenoid-rich diet in the prevention of diabetes cardiovascular complications.
Highlights
IntroductionDiabetes is a chronic low-grade inflammatory condition featured by the increased plasma levels of TNF-α, a primary mediator of inflammation and insulin resistance [2], and reactive oxygen species (ROS), both playing an important role in the promotion of endothelial dysfunction and cardiovascular complications [3]
Cardiovascular diseases represent the major complications and the main cause of reduced life expectancy in type 2 diabetic patients [1].Diabetes is a chronic low-grade inflammatory condition featured by the increased plasma levels of TNF-α, a primary mediator of inflammation and insulin resistance [2], and reactive oxygen species (ROS), both playing an important role in the promotion of endothelial dysfunction and cardiovascular complications [3].Nitric oxide is an important molecule playing a pleiotropic role in preserving vascular wall homeostasis
It diffuses to the vascular smooth muscle cells, where it activates the enzyme guanylate cyclase (GC), inducing the production of cyclic guanosine monophosphate, a molecule involved in vascular relaxation
Summary
Diabetes is a chronic low-grade inflammatory condition featured by the increased plasma levels of TNF-α, a primary mediator of inflammation and insulin resistance [2], and reactive oxygen species (ROS), both playing an important role in the promotion of endothelial dysfunction and cardiovascular complications [3]. Nitric oxide is an important molecule playing a pleiotropic role in preserving vascular wall homeostasis. It is produced by endothelial nitric oxide synthase (eNOS) via the conversion of the amino acid L-arginine into L-citrulline. Once released, it diffuses to the vascular smooth muscle cells (vSMC), where it activates the enzyme guanylate cyclase (GC), inducing the production of cyclic guanosine monophosphate (cGMP), a molecule involved in vascular relaxation. Oxidative Medicine and Cellular Longevity the maintenance of nitric oxide availability is mandatory to avoid the activation of the inflammatory process and the endothelial dysfunction
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