title: Rutoside decreases human macrophage-derived inflammatory mediators and improves clinical signs in adjuvant-induced arthritis.
abstract: BACKGROUND
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  Thus, RU may have clinical value in reducing inflammatory manifestations in human arthritis and other inflammatory diseases.
authors.affiliation: Department of Immunology and Parasitology, EA3677, School of Pharmacy, Bordeaux 2 University, 146 rue Léo Saignat, 33076 Bordeaux, France. tikauss@yahoo.fr
authors.forename: Tina
authors.initials: T
authors.lastname: Kauss
authors.forename: Daniel
authors.initials: D
authors.lastname: Moynet
authors.forename: Jérôme
authors.initials: J
authors.lastname: Rambert
authors.forename: Abir
authors.initials: A
authors.lastname: Al-Kharrat
authors.forename: Stephane
authors.initials: S
authors.lastname: Brajot
authors.forename: Denis
authors.initials: D
authors.lastname: Thiolat
authors.forename: Rachid
authors.initials: R
authors.lastname: Ennemany
authors.forename: Fawaz
authors.initials: F
authors.lastname: Fawaz
authors.forename: M Djavad
authors.initials: MD
authors.lastname: Mossalayi
mesh_terms: D000818:Animals; D001169:Arthritis, Experimental / Q000235:genetics / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology*; D001835:Body Weight / Q000187:drug effects; D002478:Cells, Cultured; D002908:Chronic Disease; D016207:Cytokines / Q000037:antagonists & inhibitors / Q000235:genetics; D004305:Dose-Response Relationship, Drug; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000037:antagonists & inhibitors*; D007375:Interleukin-1 / Q000037:antagonists & inhibitors; D008264:Macrophages / Q000187:drug effects / Q000378:metabolism*; D017737:Macrophages, Peritoneal / Q000187:drug effects / Q000378:metabolism; D009569:Nitric Oxide / Q000037:antagonists & inhibitors; D051381:Rats; D011917:Rats, Inbred Lew; D012431:Rutin / Q000008:administration & dosage / Q000494:pharmacology*; D014158:Transcription, Genetic / Q000187:drug effects; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors; D000093242:Interleukin-6 Inhibitors
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators; D007375:Interleukin-1; D009569:Nitric Oxide; D012431:Rutin; D014409:Tumor Necrosis Factor-alpha; D000093242:Interleukin-6 Inhibitors