Biological activity of anthocyanins and their phenolic degradation products and metabolites in human vascular endothelial cells
type: CreativeWork
description: Human, animal, and in vitro data indicate significant vasoprotective activity of anthocyanins. However, few studies have investigated the activity of anthocyanin degradation products and metabolites which are likely to mediate bioactivity in vivo. The present thesis therefore examined the vascular bioactivity in vitro of anthocyanins, their phenolic degradants, and the potential for interactions between dietary bioactive compounds. Seven treatment compounds (cyanidin-, peonidin-, petunidin- & malvidin-3-glucoside, and protocatechuic, vanillic, and syringic acid) and two treatment combinations (cyanidin-3-glucoside or protocatechuic acid with epicatechin, quercetin, and ascorbic acid) were screened in a human endothelial cell model for effects on endothelial nitric oxide synthase (eNOS) activity (via ELISA & colourimetric assay), and NADPH oxidase (NOX)-mediated superoxide production (by cytochrome c reduction assay, optimised in-house). A bioactive treatment was then chosen to explore possible mechanisms of NOX inhibition, namely gene expression of NOX2, NOX4, p47phox, p67phox, p22phox, & haem oxygenase-1 (HO-1), and activation/expression of p47phox and HO-1 protein; using RT-qPCR and immunoblotting (optimised for cell stimulation conditions and qPCR reference genes). Differential bioactivity of parent anthocyanins and their phenolic degradants was observed at physiologically relevant concentrations, as only anthocyanins upregulated eNOS expression (by 4- to 7-fold; p < 0.01), whereas both anthocyanins and degradants appeared to reduce endothelial superoxide levels (by 1- to 8-fold; p < 0.05). The phenolic degradant vanillic acid significantly reduced (p < 0.05) superoxide by 2-fold at 1μM, and has been reported at low micromolar levels in human serum; therefore vanillic acid was selected to elucidate pathways potentially underlying observed bioactivity. Vanillic acid did not significantly modulate expression of NOX isoforms/subunits, but an apparent induction of th…
abstract: Human, animal, and in vitro data indicate significant vasoprotective activity of anthocyanins. However, few studies have investigated the activity of anthocyanin degradation products and metabolites which are likely to mediate bioactivity in vivo. The present thesis therefore examined the vascular bioactivity in vitro of anthocyanins, their phenolic degradants, and the potential for interactions between dietary bioactive compounds. Seven treatment compounds (cyanidin-, peonidin-, petunidin- & malvidin-3-glucoside, and protocatechuic, vanillic, and syringic acid) and two treatment combinations (cyanidin-3-glucoside or protocatechuic acid with epicatechin, quercetin, and ascorbic acid) were screened in a human endothelial cell model for effects on endothelial nitric oxide synthase (eNOS) activity (via ELISA & colourimetric assay), and NADPH oxidase (NOX)-mediated superoxide production (by cytochrome c reduction assay, optimised in-house). A bioactive treatment was then chosen to explore possible mechanisms of NOX inhibition, namely gene expression of NOX2, NOX4, p47phox, p67phox, p22phox, & haem oxygenase-1 (HO-1), and activation/expression of p47phox and HO-1 protein; using RT-qPCR and immunoblotting (optimised for cell stimulation conditions and qPCR reference genes). Differential bioactivity of parent anthocyanins and their phenolic degradants was observed at physiologically relevant concentrations, as only anthocyanins upregulated eNOS expression (by 4- to 7-fold; p < 0.01), whereas both anthocyanins and degradants appeared to reduce endothelial superoxide levels (by 1- to 8-fold; p < 0.05). The phenolic degradant vanillic acid significantly reduced (p < 0.05) superoxide by 2-fold at 1μM, and has been reported at low micromolar levels in human serum; therefore vanillic acid was selected to elucidate pathways potentially underlying observed bioactivity. Vanillic acid did not significantly modulate expression of NOX isoforms/subunits, but an apparent induction of th…
author: Edwards, Michael
language: en
date published: 2013-10
date modified: 2026-07-24T02:12:03Z
provider: University of East Anglia
publisher: Networked Digital Library of Theses and Dissertations
type: WebPage
source organization: University of East Anglia