This study investigated the capacity of an anthocyanin-rich fraction (ACN-RF) from blueberry, single anthocyanins (cyanidin, delphinidin and malvidin-3-glucoside; Cy, Dp and Mv-3-glc) and related metabolites (protocatechuic, gallic and syringic acid; PrA, GA and SA) to resolve an inflammation-driven adhesion of monocytes (THP-1) on endothelial cell (HUVECs) and secretion of cell adhesion molecules E-selectin and vascular cell adhesion molecule 1 (VCAM-1). The adhesion of THP-1 to HUVECs was induced by tumour necrosis factor α (TNF-α, 100 ng mL-1). Subsequently, ACN-RF, single ACNs and metabolites (from 0.01 to 10 μg mL-1) were incubated for 24 h. The adhesion was measured in a fluorescence spectrophotometer. E-selectin and VCAM-1 were quantified by ELISA. No toxicological effects were observed for the compounds and the doses tested. ACN-RF and Mv-3-glc reducedTHP-1 adhesion at all the concentrations with the maximum effect at 10 μg/ml (-60.2% for ACNs and-33.9% for Mv-3-glc). Cy-3-glc decreased the adhesion by about 41.8% at 10 μg mL-1, while PrA and GA reduced the adhesion of THP-1 to HUVECs both at 1 and at 10 μg mL-1 (-29.5% and -44.3% for PrA, respectively, and -18.0%and -59.3% for GA, respectively). At the same concentrations a significant reduction of E-selectin, but notVCAM-1 levels, was documented. No effect was observed following Dp-3-glc and SA supplementation. Overall, ACNs and metabolites seem to resolve, in a dose-dependent manner, the inflammation-driven adhesion of THP-1 to HUVECs by decreasing E-selectin concentrations. Interestingly, Mv-3-glc was active at physiologically relevant concentrations.
Anthocyanins and metabolites resolve TNF-α-mediated production of E-selectin and adhesion of monocytes to endothelial cells / C. Del Bo', M. Marino, P. Riso, P. Møller, M. Porrini. - In: CHEMICO-BIOLOGICAL INTERACTIONS. - ISSN 0009-2797. - 300(2019 Feb 25), pp. 49-55.
Anthocyanins and metabolites resolve TNF-α-mediated production of E-selectin and adhesion of monocytes to endothelial cells
C. Del Bo'Primo
;M. MarinoSecondo
;P. Riso
;M. PorriniUltimo
2019
Abstract
This study investigated the capacity of an anthocyanin-rich fraction (ACN-RF) from blueberry, single anthocyanins (cyanidin, delphinidin and malvidin-3-glucoside; Cy, Dp and Mv-3-glc) and related metabolites (protocatechuic, gallic and syringic acid; PrA, GA and SA) to resolve an inflammation-driven adhesion of monocytes (THP-1) on endothelial cell (HUVECs) and secretion of cell adhesion molecules E-selectin and vascular cell adhesion molecule 1 (VCAM-1). The adhesion of THP-1 to HUVECs was induced by tumour necrosis factor α (TNF-α, 100 ng mL-1). Subsequently, ACN-RF, single ACNs and metabolites (from 0.01 to 10 μg mL-1) were incubated for 24 h. The adhesion was measured in a fluorescence spectrophotometer. E-selectin and VCAM-1 were quantified by ELISA. No toxicological effects were observed for the compounds and the doses tested. ACN-RF and Mv-3-glc reducedTHP-1 adhesion at all the concentrations with the maximum effect at 10 μg/ml (-60.2% for ACNs and-33.9% for Mv-3-glc). Cy-3-glc decreased the adhesion by about 41.8% at 10 μg mL-1, while PrA and GA reduced the adhesion of THP-1 to HUVECs both at 1 and at 10 μg mL-1 (-29.5% and -44.3% for PrA, respectively, and -18.0%and -59.3% for GA, respectively). At the same concentrations a significant reduction of E-selectin, but notVCAM-1 levels, was documented. No effect was observed following Dp-3-glc and SA supplementation. Overall, ACNs and metabolites seem to resolve, in a dose-dependent manner, the inflammation-driven adhesion of THP-1 to HUVECs by decreasing E-selectin concentrations. Interestingly, Mv-3-glc was active at physiologically relevant concentrations.File | Dimensione | Formato | |
---|---|---|---|
Del Bo' et al., post_print.pdf
accesso aperto
Descrizione: Articolo Principale
Tipologia:
Pre-print (manoscritto inviato all'editore)
Dimensione
751.45 kB
Formato
Adobe PDF
|
751.45 kB | Adobe PDF | Visualizza/Apri |
Del Bo' C 2019 Chemico_Biolog Interct.pdf
accesso riservato
Descrizione: Articolo Principale
Tipologia:
Publisher's version/PDF
Dimensione
3.98 MB
Formato
Adobe PDF
|
3.98 MB | Adobe PDF | Visualizza/Apri Richiedi una copia |
Pubblicazioni consigliate
I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.