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Anti-inflammatory action of quercetin

The anti-inflammatory action of quercetin is caused by the inhibition of enzymes, such as lipoxygenase, and the inhibition of inflammatory mediators. Quercetin also inhibits the release of histamine, which causes congestion, by basophils and mast cells.

Polychlorinated biphenyls (PCBs) exert their toxic effect by binding to the aryl hydrocarbon receptor, resulting in the disruption of cell function by altering the transcription of genes. One study conducted at the University of Kentucky, USA, showed that treatment of endothelial cells with quercetin significantly reduced the expression of pro-inflammatory genes induced by polychlorinated biphenyls (PCBs) [1]. The researchers also found that the flavonoid downregulated the inflammatory pathways through mechanisms associated with functional caveolae.

A study by the Niger Delta University investigated the inhibitory effect of quercetin and its metabolite 3-O-methyl quercetin on lipopolysaccharide-mediated activation of macrophage cells [2]. The scientists measured inflammatory markers (catalase activity, nitric oxide, tumour necrosis factor-alpha, interleukin 6 and interleukin 1) of the supernatant of cell cultures exposed to lipopolysaccharide and quercetin or 3-O-methyl quercetin. They found that Both quercetin and 3-O-methyl quercetin (at 30 mM) reduced the levels of all the markers with 3-O-methyl quercetin showed a stronger effect that quercetin. Tang and co-workers also found that quercetin attenuated the release late pro-inflammatory mediator HMGB1 in animals with established endotoxemia [3]. Their in-vitro test with macrophages confirmed that quercetin inhibited release as well as the cytokine activities of HMGB1.

Scientists of the University of Maastricht, The Netherlands, could not demonstrate an anti-inflammatory effect of quercetin in an intervention study [4]. After treating volunteers during 4 weeks with quercetin they found no influence on lipopolysaccharide-induced tumor necrosis factor-alpha levels, although total plasma antioxidant status was increased. Their in-vitro study with blood in the test tube showed that quercetin dose-dependently inhibited lipopolysaccharide-induced tumor necrosis factor-alpha production. The lack of effect in this intervention study was probably caused by low cytokine and high antioxidant levels at baseline, indicating that neither inflammation nor oxidative stress was present. They concluded that only patients with increased levels of inflammation and oxidative stress might benefit from a quercetin supplementation.

Quercetin exerts its anti-inflammatory action in epithelial cells through mechanisms that inhibit cofactor recruitment at the chromatin of pro-inflammatory genes. Ruiz and co-workers at the Technical University of Munich came to this conclusion after studying the effect of quercetin and its enteric bacterial metabolites, taxifolin, alphitonin, and 3, 4-dihydroxy-phenylacetic acid in small intestinal epithelial cell of mice with experimental ileitis [5].

[1] Quercetin blocks caveolae-dependent pro-inflammatory responses induced by co-planar PCBs. Environ Int. 2009 Jul 14.
[2] Inhibitory activity of quercetin and its metabolite on lipopolysaccharide-induced activation of macrophage U937 cells. Food Chem Toxicol. 2009 Apr;47(4):809-12.
[3] Quercetin Prevents Lipopolysaccharide-induced HMGB1 Release and Proinflammatory Function. Am J Respir Cell Mol Biol. 2009 Mar 5.
[4] In vitro and ex vivo anti-inflammatory activity of quercetin in healthy volunteers. Nutrition. 2008 Jul-Aug;24(7-8):703-10.
[5] Quercetin inhibits TNF-induced NF-kappaB transcription factor recruitment to proinflammatory gene promoters in murine intestinal epithelial cells. J Nutr. 2007 May;137(5):1208-15.

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