Rutoside decreases human macrophage-derived inflammatory mediators and improves clinical signs in adjuvant-induced arthritis

Dietary flavonols may play an important role in the adjunct therapy of chronic inflammation. The availability of therapeutic formulations of pentahydroxyflavone glycoside, rutoside (RU), led us to investigate the ability of this molecule to modulate the release of various proinflammatory mediators f...

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Veröffentlicht in:Arthritis research & therapy 2008-01, Vol.10 (1), p.R19-R19, Article R19
Hauptverfasser: Kauss, Tina, Moynet, Daniel, Rambert, Jérôme, Al-Kharrat, Abir, Brajot, Stephane, Thiolat, Denis, Ennemany, Rachid, Fawaz, Fawaz, Mossalayi, M Djavad
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container_issue 1
container_start_page R19
container_title Arthritis research & therapy
container_volume 10
creator Kauss, Tina
Moynet, Daniel
Rambert, Jérôme
Al-Kharrat, Abir
Brajot, Stephane
Thiolat, Denis
Ennemany, Rachid
Fawaz, Fawaz
Mossalayi, M Djavad
description Dietary flavonols may play an important role in the adjunct therapy of chronic inflammation. The availability of therapeutic formulations of pentahydroxyflavone glycoside, rutoside (RU), led us to investigate the ability of this molecule to modulate the release of various proinflammatory mediators from human activated macrophages in vitro and to ameliorate arthritic markers in a rat model. RU was added simultaneously to human macrophages during their activation. Cells were then analyzed for inflammation-related gene expression using a specific array, and cell supernatants were collected to measure inflammatory mediators. RU was also injected into adjuvant-induced arthritic rats, and disease progression and body weight were evaluated until 50 days after injection. Sera and peritoneal macrophages were also collected to quantify the RU effect on various inflammatory markers. RU inhibited inflammation-related gene expression in activated human macrophages and the release of nitric oxide, tumor necrosis factor-alpha, interleukin (IL)-1, and IL-6 from these cells. In a rat model, RU inhibited clinical signs of chronic arthritis, correlating with decreased levels of inflammatory cytokines detected in rat sera and macrophage supernatants. Thus, RU may have clinical value in reducing inflammatory manifestations in human arthritis and other inflammatory diseases.
doi_str_mv 10.1186/ar2372
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The availability of therapeutic formulations of pentahydroxyflavone glycoside, rutoside (RU), led us to investigate the ability of this molecule to modulate the release of various proinflammatory mediators from human activated macrophages in vitro and to ameliorate arthritic markers in a rat model. RU was added simultaneously to human macrophages during their activation. Cells were then analyzed for inflammation-related gene expression using a specific array, and cell supernatants were collected to measure inflammatory mediators. RU was also injected into adjuvant-induced arthritic rats, and disease progression and body weight were evaluated until 50 days after injection. Sera and peritoneal macrophages were also collected to quantify the RU effect on various inflammatory markers. RU inhibited inflammation-related gene expression in activated human macrophages and the release of nitric oxide, tumor necrosis factor-alpha, interleukin (IL)-1, and IL-6 from these cells. 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The availability of therapeutic formulations of pentahydroxyflavone glycoside, rutoside (RU), led us to investigate the ability of this molecule to modulate the release of various proinflammatory mediators from human activated macrophages in vitro and to ameliorate arthritic markers in a rat model. RU was added simultaneously to human macrophages during their activation. Cells were then analyzed for inflammation-related gene expression using a specific array, and cell supernatants were collected to measure inflammatory mediators. RU was also injected into adjuvant-induced arthritic rats, and disease progression and body weight were evaluated until 50 days after injection. Sera and peritoneal macrophages were also collected to quantify the RU effect on various inflammatory markers. RU inhibited inflammation-related gene expression in activated human macrophages and the release of nitric oxide, tumor necrosis factor-alpha, interleukin (IL)-1, and IL-6 from these cells. 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subjects Animals
Arthritis
Arthritis, Experimental - genetics
Arthritis, Experimental - metabolism
Arthritis, Experimental - pathology
Arthritis, Experimental - physiopathology
Body Weight - drug effects
Care and treatment
Cells, Cultured
Chronic Disease
Cytokines - antagonists & inhibitors
Cytokines - genetics
Dose-Response Relationship, Drug
Female
Health aspects
Humans
Inflammation
Inflammation Mediators - antagonists & inhibitors
Interleukin-1 - antagonists & inhibitors
Interleukin-6 - antagonists & inhibitors
Macrophages - drug effects
Macrophages - metabolism
Macrophages, Peritoneal - drug effects
Macrophages, Peritoneal - metabolism
Nitric Oxide - antagonists & inhibitors
Rats
Rats, Inbred Lew
Rutin - administration & dosage
Rutin - pharmacology
Transcription, Genetic - drug effects
Tumor Necrosis Factor-alpha - antagonists & inhibitors
title Rutoside decreases human macrophage-derived inflammatory mediators and improves clinical signs in adjuvant-induced arthritis
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