quercetin-3--sulfate has been researched along with 3-methylquercetin* in 4 studies
4 other study(ies) available for quercetin-3--sulfate and 3-methylquercetin
Article | Year |
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Effects of Quercetin Metabolites on Triglyceride Metabolism of 3T3-L1 Preadipocytes and Mature Adipocytes.
Quercetin (Q) has rapid metabolism, which may make it worthwhile to focus on the potential activity of its metabolites. Our aim was to evaluate the triglyceride-lowering effects of Q metabolites in mature and pre-adipocytes, and to compare them to those induced by Q. 3T3-L1 mature and pre-adipocytes were treated with 0.1, 1 and 10 µM of Q, tamarixetin (TAM), isorhamnetin (ISO), quercetin-3- Topics: 3T3-L1 Cells; Adipocytes; Animals; Cell Differentiation; Disaccharides; Dose-Response Relationship, Drug; Fatty Acids, Nonesterified; Gene Expression Profiling; Gene Expression Regulation; Glycerol; Lipid Metabolism; Mice; Quercetin; Triglycerides | 2019 |
Effects of physiological quercetin metabolites on interleukin-1β-induced inducible NOS expression.
Cytokines released by inflammatory cells around the pancreatic islets are implicated in the pathogenesis of diabetes mellitus. Specifically, interleukin-1β (IL-1β) is known to be involved in islet β-cell damage by activation of nuclear factor-κB (NF-κB)-mediated inducible nitric oxide synthase (iNOS) gene expression. Though most flavonoids are shown to have various beneficial effects, little is known about the anti-inflammatory effects of their metabolites. Therefore, we investigated the effects of quercetin and its metabolites quercetin 3'-sulfate, quercetin 3-glucuronide and isorhamnetin 3-glucuronide on IL-1β-stimulated iNOS gene expression in RINm5F β-cells. The nitrite level, iNOS protein and its mRNA expression levels and iNOS promoter activity were measured. In addition, IκBα protein phosphorylation, nuclear translocation of nuclear factor-κB (NF-κB) and NF-κB DNA binding activity were determined. Adenosine 5'-triphosphate disodium salt-induced insulin release was also measured. Quercetin significantly reduced IL-1β-induced nitrite production, iNOS protein and its mRNA expression levels, and it also inhibited IL-1β-induced IκBα phosphorylation, NF-κB activation and iNOS promoter activity. Additionally, quercetin significantly restored the inhibition of insulin secretion by IL-1β. Meanwhile, quercetin metabolites did not show any effect on IL-1β-induced iNOS gene expression and also on insulin secretion. Therefore, in terms of iNOS expression mechanism, dietary ingestion of quercetin is unlikely to show anti-inflammatory effects in rat islet β-cells exposed to IL-1β. Topics: Animals; Cells, Cultured; Gene Expression Regulation, Enzymologic; I-kappa B Proteins; Insulin; Insulin Secretion; Interleukin-1beta; Islets of Langerhans; NF-kappa B; Nitric Oxide Synthase Type II; Nitrites; Phosphorylation; Promoter Regions, Genetic; Quercetin; Rats | 2012 |
Glucuronidated and sulfated metabolites of the flavonoid quercetin prevent endothelial dysfunction but lack direct vasorelaxant effects in rat aorta.
Epidemiological studies have reported an inverse association between dietary flavonoid intake and mortality for ischemic heart disease. Quercetin reduces blood pressure and restores endothelial dysfunction in hypertensive animals. However, quercetin (aglycone) is usually not present in plasma, but it is rapidly metabolized during absorption by methylation, glucuronidation and sulfation. We have analyzed the vasorelaxant effects and the role on NO bioavailability and endothelial function of quercetin and its conjugated metabolites (quercetin-3-glucuronide, isorhamnetin-3-glucuronide and quercetin-3'-sulfate) in rat aorta. Thoracic aortic rings isolated from Wistar rats were mounted for isometric force recording and endothelial function was tested by measuring the vasorelaxant response to acetylcholine. NADPH-enhanced O(2)(-) release was quantified in homogenates from cultured aortic smooth muscle cells using lucigenin chemiluminescence. Unlike quercetin, the conjugated metabolites had no direct vasorelaxant effect, and did not modify endothelial function or the biological activity of NO. However, all metabolites (at 10 micromol/L) prevented, at least partially, the impairment of endothelial-derived NO response under conditions of high oxidative stress induced by the SOD inhibitor DETCA. Furthermore, they protected the biological activity of exogenous NO when impaired by DETCA. Quercetin and quercetin-3'-sulfate (>or=10 micromol/L) or quercetin-3-glucuronide (100 micromol/L) inhibited NADPH oxidase-derived O(2)(-) release. Quercetin and quercetin-3-glucuronide (1 micromol/L) prevented the endothelial dysfunction induced by incubation with ET-1. These data indicate, for the first time, that the conjugated metabolites could be responsible for the in vivo protective activity of quercetin on endothelial dysfunction. Topics: Acetylcholine; Animals; Antioxidants; Aorta, Thoracic; Biotransformation; Dose-Response Relationship, Drug; Endothelin-1; Endothelium, Vascular; Flavonols; Glucuronides; In Vitro Techniques; NADPH Oxidases; Nitric Oxide; Oxidative Stress; Quercetin; Rats; Rats, Wistar; Sulfates; Superoxides; Vasodilation; Vasodilator Agents | 2009 |
Physiologically relevant metabolites of quercetin have no effect on adhesion molecule or chemokine expression in human vascular smooth muscle cells.
Dietary flavonoids have been shown to have a number of anti-inflammatory properties, including decreasing the expression of adhesion molecules. Flavonoids however, are metabolised during absorption and the forms reaching the systemic circulation are glucuronidated, sulfated and methylated. Most previous studies of the effects of flavonoids have used the parent compounds rather than the metabolites found in blood plasma and we have recently shown that metabolites of quercetin can retain some of the anti-inflammatory properties of the parent aglycone when used to treat human umbilical endothelial cells (HUVEC). Using both physiologically achievable (2 microM) and supraphysiological (10 microM) concentrations, we investigated the ability of quercetin and its predominant human metabolites to attenuate the expression of vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1) and monocyte chemoattractant protein-1 (MCP-1) in human umbilical artery smooth muscle cells (HUASMC) activated by tumor necrosis factor-alpha (TNFalpha). Quercetin was able to reduce TNFalpha-induced upregulation of VCAM-1, ICAM-1 and MCP-1 at both the protein and transcript (mRNA) level in HUASMC. However the quercetin metabolites, quercetin 3'-sulfate, quercetin 3-glucuronide and 3'-methylquercetin 3-glucuronide, had no effect on TNFalpha-induced up regulation of adhesion molecule or chemokine expression, at either concentration tested. These data do not support the notion that the vascular anti-inflammatory effects of quercetin consumption are mediated through effects on smooth muscle cells. Topics: Cell Division; Cell Survival; Cells, Cultured; Chemokine CCL2; Chemokines; Flavonols; Gene Expression; Humans; Intercellular Adhesion Molecule-1; Muscle, Smooth, Vascular; Myocytes, Smooth Muscle; Quercetin; RNA, Messenger; Tumor Necrosis Factor-alpha; Umbilical Arteries; Vascular Cell Adhesion Molecule-1 | 2009 |