In vivo quercitrin anti‐inflammatory effect involves release of quercetin, which inhibits inflammation through down‐regulation of the NF‐κB pathway

Quercetin is a common antioxidant flavonoid found in vegetables, which is usually present in glycosylated forms, such as quercitrin (3‐rhamnosylquercetin). Previous in vitro experiments have shown that quercetin exerts a bigger effect than quercitrin in the down‐regulation of the inflammatory respon...

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Veröffentlicht in:European journal of immunology 2005-02, Vol.35 (2), p.584-592
Hauptverfasser: Comalada, Mònica, Camuesco, Desirée, Sierra, Saleta, Ballester, Isabel, Xaus, Jordi, Gálvez, Julio, Zarzuelo, Antonio
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container_title European journal of immunology
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creator Comalada, Mònica
Camuesco, Desirée
Sierra, Saleta
Ballester, Isabel
Xaus, Jordi
Gálvez, Julio
Zarzuelo, Antonio
description Quercetin is a common antioxidant flavonoid found in vegetables, which is usually present in glycosylated forms, such as quercitrin (3‐rhamnosylquercetin). Previous in vitro experiments have shown that quercetin exerts a bigger effect than quercitrin in the down‐regulation of the inflammatory response. However, such results have not been reproduced in in vivo experimental models of intestinal inflammation, in which quercetin did not show beneficial effects while its glycosides, quercitrin or rutin, have demonstrated their effectiveness. In this study, we have reported that the in vivo effects of quercitrin in the experimental model of rat colitis induced by dextran sulfate sodium can be mediated by the release of quercetin generated after glycoside's cleavage by the intestinal microbiota. This is supported by the fact that quercetin, but not quercitrin, is able to down‐regulate the inflammatory response of bone marrow‐derived macrophages in vitro. Moreover, we have demonstrated that quercetin inhibits cytokine and inducible nitric oxide synthase expression through inhibition of the NF‐κB pathway without modification of c‐Jun N‐terminal kinase activity (both in vitro and in vivo). As a conclusion, our report suggests that quercitrin releases quercetin in order to perform its anti‐inflammatory effect which is mediated through the inhibition of the NF‐κB pathway.
doi_str_mv 10.1002/eji.200425778
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Previous in vitro experiments have shown that quercetin exerts a bigger effect than quercitrin in the down‐regulation of the inflammatory response. However, such results have not been reproduced in in vivo experimental models of intestinal inflammation, in which quercetin did not show beneficial effects while its glycosides, quercitrin or rutin, have demonstrated their effectiveness. In this study, we have reported that the in vivo effects of quercitrin in the experimental model of rat colitis induced by dextran sulfate sodium can be mediated by the release of quercetin generated after glycoside's cleavage by the intestinal microbiota. This is supported by the fact that quercetin, but not quercitrin, is able to down‐regulate the inflammatory response of bone marrow‐derived macrophages in vitro. Moreover, we have demonstrated that quercetin inhibits cytokine and inducible nitric oxide synthase expression through inhibition of the NF‐κB pathway without modification of c‐Jun N‐terminal kinase activity (both in vitro and in vivo). As a conclusion, our report suggests that quercitrin releases quercetin in order to perform its anti‐inflammatory effect which is mediated through the inhibition of the NF‐κB pathway.</description><identifier>ISSN: 0014-2980</identifier><identifier>EISSN: 1521-4141</identifier><identifier>DOI: 10.1002/eji.200425778</identifier><language>eng</language><publisher>Weinheim: WILEY‐VCH Verlag</publisher><subject>Inflammation ; Monocytes/macrophages ; Mucosa ; Signal transduction</subject><ispartof>European journal of immunology, 2005-02, Vol.35 (2), p.584-592</ispartof><rights>Copyright © 2005 WILEY‐VCH Verlag GmbH &amp; Co. 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subjects Inflammation
Monocytes/macrophages
Mucosa
Signal transduction
title In vivo quercitrin anti‐inflammatory effect involves release of quercetin, which inhibits inflammation through down‐regulation of the NF‐κB pathway
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