Modification of low-density lipoproteins by flavonoids

Whalley, Catherine V. de; Rankin, Sara M.; Hoult, J.R.S.; Jessup, Wendy; Wilkins, Gary M.; Collard, Jane; Leake, David S.

doi:10.1042/bst0181172

Cited by 11 publications

(6 citation statements)

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“…Flavonoids, polyphenolic compounds of the human diet, are also radical scavengers that may suppress LDL oxidation and inflammatory progression in the artery wall. Certain flavonoids, such as morin, fisetin, quercetin, and gossypetin, were shown to inhibit the oxidative modification of LDL by MACs, at least partly by conserving the ␣-tocopherol content of the LDL particles (31). The positive effects of flavonoids have been attributed to competitive inhibition of cyclic nucleotide phosphodiesterase (PDE), an elevation in cAMP level, and subsequent activation of protein kinase A (cAMP-dependent protein kinase), which targets lipid droplet-associated lipases and activates rehydrolysis of triglycerides and cholesteryl esters (115).…”

Section: Antioxidants and Scavengers Affecting Mac Redox Statusmentioning

confidence: 99%

Role of Redox Regulation and Lipid Rafts in Macrophages During Ox-LDL–Mediated Foam Cell Formation

Schmitz

Grandl

2007

Antioxidants & Redox Signaling

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Hyperlipidemias and small dense LDLs in patients with high-triglyceride low-HDL syndromes lead to a prolonged half life of apoB-containing particles. This is associated with reactive oxygen species (ROS) activation and leads to formation of oxidized LDL (Ox-LDL). Generators of ROS in macrophages (MACs) include myeloperoxidase (MPO)-mediated respiratory burst and raft-associated NADPH-oxidase. The intracellular oxidant milieu is involved in cellular signaling pathways, like ion-transport systems, protein phosphorylation, and gene expression. Lipid oxidation through ROS can amplify foam cell formation through Ox-LDL uptake, leading to formation of ceramide (Cer)-rich lipid membrane microdomains, and is associated with expansion of the lysosomal compartment and an upregulation of ABCA1 and other genes of the AP3 secretory pathway. Ox-LDL may also affect cell-surface turnover of Cer-backbone sphingolipids and apoE-mediated uptake by LRP-family members. In contrast, HDL-mediated lipid efflux causes disruption of lipid membrane microdomains and prevents foam cell formation. Oxidation of HDL through MPO leads to a failure of lipid efflux and enhancement of MAC loading. Therefore, lipid rafts and oxidation processes are important in regulation of MAC foam cell formation and atherosclerosis, and the balance between oxidant and antioxidant intracellular systems is critically important for efficient MAC function.

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Section: Antioxidants and Scavengers Affecting Mac Redox Statusmentioning

confidence: 99%

Role of Redox Regulation and Lipid Rafts in Macrophages During Ox-LDL–Mediated Foam Cell Formation

Schmitz

Grandl

2007

Antioxidants & Redox Signaling

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“…Onions, apples, tea and red wine are important sources of quercetin in the human diet [1,2]. Quercetin exhibits a wide range of biological effects including inhibition of low-density lipoprotein oxidation and platelet aggregation as well as improvement of endothelial function [3][4][5]. Cell culture and animal studies suggest potential antiinflammatory properties of quercetin [6][7][8].…”

Section: Introductionmentioning

confidence: 98%

Effect of quercetin and its metabolites isorhamnetin and quercetin-3-glucuronide on inflammatory gene expression: role of miR-155

Boesch-Saadatmandi

Łoboda

Wagner

et al. 2011

The Journal of Nutritional Biochemistry

223

178

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“…19 Flavonoids are also ROS scavengers and inhibitors of LDL oxidation. 20 In addition, flavonoids inhibit several ROS generating enzymes including xanthine oxidase 21 and the NADPH oxidase complex in neutrophils. 22 In platelets, quercetin also inhibited NADPH oxidase when stimulated by protein kinase C (PKC), an effect that could be explained by either the well-known inhibitory effects of flavonoids on PKC or by a direct inhibitory effect on NADPH oxidase.…”

Section: Introductionmentioning

confidence: 99%

Quercetin and its metabolites inhibit the membrane NADPH oxidase activity in vascular smooth muscle cells from normotensive and spontaneously hypertensive rats

et al. 2015

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Quercetin, the most abundant dietary flavonol, exerts antioxidant effects reducing vascular superoxide (O2(-)) and improving endothelial function in animal models of cardiovascular disease. Herein we evaluated the effects of quercetin, and its plasma metabolites, on the nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase activity, the main source of O2(-) in the vessel wall, in vascular smooth muscle cells (VSMCs) from spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY). Quercetin and its metabolites isorhamnetin and kaempferol inhibited the NADPH-stimulated lucigenin-chemiluminescence signal in VSMCs from both strains. The inhibitory effect of quercetin-3-glucuronide increased after prolonged incubation and was inhibited in the presence of the β-glucuronidase inhibitor saccharolactone. These effects were unrelated to their O2(-) scavenging properties, since they induced only a small inhibition of the rate of pyrogallol autoxidation at high concentrations. All bioflavonoids tested acted as non-competitive inhibitors with respect to NADPH. In conclusion, quercetin and its metabolites inhibit the NADPH oxidase activity in VSMCs reducing O2(-) generation more efficiently than their effect as O2(-) scavengers. The effect of quercetin-3-glucuronide was due to deconjugation and release of free quercetin. The effect is similar in VSMCs from normotensive and hypertensive animals.

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Modification of low-density lipoproteins by flavonoids

Cited by 11 publications

References 0 publications

Role of Redox Regulation and Lipid Rafts in Macrophages During Ox-LDL–Mediated Foam Cell Formation

Role of Redox Regulation and Lipid Rafts in Macrophages During Ox-LDL–Mediated Foam Cell Formation

Effect of quercetin and its metabolites isorhamnetin and quercetin-3-glucuronide on inflammatory gene expression: role of miR-155

Quercetin and its metabolites inhibit the membrane NADPH oxidase activity in vascular smooth muscle cells from normotensive and spontaneously hypertensive rats

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