title: Effects of peroxisome proliferator-activated receptors-gamma ligands on dextran sodium sulphate-induced colitis in rats.
abstract: Recent studies indicate the involvement of peroxisone proliferator-activated receptor-γ (PPAR-γ) in the inflammatory reaction. The exact mechanism of PPAR-γ action has not been elucidated. It is supposed that PPAR-γ regulates transcription of genes responsible for encoding cytokines involved in the inflammatory response. The latest studies, carried out to explain the pathogenesis of non-specific colitis, confirm beneficial effects of PPAR-γ agonists on attenuation of colon inflammation. The aim of the present study was to assess the effects of nuclear PPAR-γ activity on the course of experimental acute colitis induced by intragastric administration of dextran sodium sulphate (DSS) using the PPAR-γ agonist rosiglitazone and the antagonist BADGE in rats. Colitis in Wistar rats was induced by 1.5% DSS administered in drinking water for 8 days. Animals with induced colitis received rosiglitazone, bisphenol A diglycidyl ether (BADGE) or both substances. After decapitation, colons were macroscopically and histopathologically evaluated. Levels of interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-10 (IL-10), tumor necrosis factor-α (TNF-α) and myeloperoxidase (MPO) were determined in serum and colon homogenates using ELISA. In rats with experimentally induced colitis receiving rosiglitazone, the inflammatory reaction was found to be markedly limited; ulceration, oedema and infiltration activity were reduced. The activated PPAR-γ inhibit the expression of proinflammatory factors, such as IL-6, TNF-α, and neutrophil chemotaxis, which was evidenced by MPO reduction in serum and colon homogenates mediated by rosiglitazone. The positive effects of rosiglitazone on expression of IL-10 were also demonstrated. During the short period of observation, BADGE did not increase histopathological inflammatory markers.
authors: Department of Gastroenterology, Medical University of Lublin, Poland. celinski.krzysztof@gmail.com
authors: K
authors: K
authors: Celinski
authors: T
authors: T
authors: Dworzanski
authors: A
authors: A
authors: Korolczuk
authors: R
authors: R
authors: Piasecki
authors: M
authors: M
authors: Slomka
authors: A
authors: A
authors: Madro
authors: R
authors: R
authors: Fornal
mesh_terms: D000818:Animals; D001522:Behavior, Animal; D001559:Benzhydryl Compounds; D002273:Carcinogens / Q000494:pharmacology; D003092:Colitis / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology*; D003106:Colon / Q000166:cytology / Q000378:metabolism / Q000473:pathology*; D016207:Cytokines / Q000097:blood; D016264:Dextran Sulfate / Q000633:toxicity; D004852:Epoxy Compounds / Q000494:pharmacology; D007004:Hypoglycemic Agents / Q000494:pharmacology; D007413:Intestinal Mucosa / Q000033:anatomy & histology / Q000378:metabolism / Q000473:pathology; D007420:Intestine, Large / Q000033:anatomy & histology / Q000473:pathology*; D008024:Ligands; D047495:PPAR gamma / Q000819:agonists / Q000037:antagonists & inhibitors / Q000378:metabolism*; D009195:Peroxidase / Q000097:blood; D051381:Rats; D017208:Rats, Wistar; D000077154:Rosiglitazone; D045162:Thiazolidinediones / Q000494:pharmacology; D000098826:Bisphenol A Compounds
chemical_list: D001559:Benzhydryl Compounds; D002273:Carcinogens; D016207:Cytokines; D016264:Dextran Sulfate; D004852:Epoxy Compounds; D007004:Hypoglycemic Agents; D008024:Ligands; D047495:PPAR gamma; D009195:Peroxidase; D000077154:Rosiglitazone; D045162:Thiazolidinediones; C019273:bisphenol A diglycidyl ether; D000098826:Bisphenol A Compounds