PPAR-Gamma Agonist Rosiglitazone Attenuates the Inflammation Caused by Carrageenan in the Mouse Model of Pleurisy

• Published in: Inflammation Vol. 35; no. 1; pp. 280 - 288
• Main Authors: da Silva Buss, Ziliani, Medeiros, Yara S., Fröde, Tania S.
• Format: Journal Article
• Language: English
• Published: Boston Springer US 01-02-2012; Springer Nature B.V
• Subjects: Adenosine Deaminase - metabolism; Animals; Biomedical and Life Sciences; Biomedicine; Carrageenan; Cell Movement; Disease Models, Animal; Immunology; Inflammation - chemically induced; Inflammation - drug therapy; Inflammation - pathology; Inflammation Mediators - metabolism; Interleukin-17 - metabolism; Interleukin-1beta - metabolism; Internal Medicine; Leukocytes, Mononuclear - metabolism; Mice; Pathology; Peroxidase - metabolism; Pharmacology/Toxicology; Pleurisy - chemically induced; Pleurisy - drug therapy; Pleurisy - immunology; PPAR gamma - agonists; Rheumatology; Thiazolidinediones - pharmacology; Tumor Necrosis Factor-alpha - metabolism; Vascular Endothelial Growth Factor A - metabolism; rosiglitazone; cytokines; anti-inflammatory effect; pro-inflammatory mediators; pleurisy
• ISSN: 0360-3997; 1573-2576
• DOI: 10.1007/s10753-011-9316-6

The aim of this study was to investigate the anti-inflammatory efficacy of rosiglitazone (ROSI) in a pleurisy model of carrageenan-induced inflammation. Efficacy was monitored in the mouse pleural cavity by evaluating leukocyte migration, exudate concentration, and myeloperoxidase (MPO) and adenosine deaminase (ADA) activities concomitantly with nitrate/nitrite (NOx), tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), interleukin-17A (IL-17A), and vascular endothelial growth factor-alpha (VEGF-α) levels 4 and 48 h after pleurisy induction. In both phases (4 and 48 h) of pleurisy, ROSI inhibited all the inflammation parameters that were tested (
p
 < 0.05). These results provide evidence that ROSI was efficacious in inhibiting pro-inflammatory mediators. These anti-inflammatory effects are assumed to mainly result from the inhibition of products released from activated leukocytes, such as MPO, ADA, NOx, TNF-α, IL-1β, IL-17A, and VEGF-α.