Activated and inactivated PPARs-gamma modulate experimentally induced colitis in rats
| Autor: | Krzysztof Celiński, Agnieszka Madro, Sebastian Radej, Halina Cichoż-Lach, Agnieszka Korolczuk, Maria Słomka, Tomasz Dworzanski |
|---|---|
| Rok vydání: | 2011 |
| Předmět: |
PPAR-γ
medicine.medical_specialty Colon Inflammation Inflammatory bowel disease Proinflammatory cytokine rosiglitazone chemistry.chemical_compound Internal medicine medicine Animals Rats Wistar Colitis Bisphenol A diglycidyl ether Peroxidase IL-6 biology Interleukin-6 Tissue Extracts Body Weight Antagonist Organ Size General Medicine medicine.disease Interleukin-10 Rats PPAR gamma Basic Research Endocrinology chemistry BADGE Myeloperoxidase IL-10 Immunology biology.protein medicine.symptom Rosiglitazone medicine.drug |
| Zdroj: | Medical Science Monitor : International Medical Journal of Experimental and Clinical Research |
| ISSN: | 1234-1010 |
| DOI: | 10.12659/msm.881712 |
| Popis: | Summary Background This study sought to define the mechanism by which PPAR-γ ligands affect the course of experimentally induced colitis in rats. Material/Methods Inflammation was induced in Wistar rats by a single rectal administration of 2,4,6,-trinitrobenzene sulfonic acid (TNBS). The antagonist of PPARγ antagonist, bisphenol A diglycidyl ether (BADGE), was administrated intraperitoneally 120 mg/kg 4 times every other day. Rosiglitazone 8 mg/kg was administrated by gastric tube 4 times. Body weight was measured daily. After killing, the large intestinal tissue was weighed and collected for histopathologic and immunoenzymatic tests. Levels of IL-6, IL-10, and myeloperoxidase (MPO) were determined in serum and in intestinal homogenates. Results Rats receiving rosiglitazone had higher body weight, whereas large intestine weight/length ratio was lower; histology showed fewer inflammatory markers. Rats receiving TNBS and TNBS along with BADGE had more intensive inflammatory changes. Rosiglitazone alone decreased expression of IL-6; used with TNBS it decreased expression of MPO in intestinal tissue, yet did not increase the expression of IL-10. Decreased levels of MPO indicate reduced neutrophil-dependent immune response. The antagonist of PPAR-γ increased IL-6 in serum and decreased IL-10 in intestinal homogenates. Bisphenol A diglycidyl ether administrated to healthy animals increases serum IL-6 levels. Conclusions Rosiglitazone inhibits experimental inflammation; administration of its selective antagonist abolishes this protective influence. Rosiglitazone inhibits expression of proinflammatory IL-6 and does not affect IL-10. Agonists of PPARs-γ are possibilities for inflammatory bowel disease prevention. Exogenous substances blocking PPARs-γ may contribute to development or relapse of nonspecific inflammatory bowel diseases. |
| Databáze: | OpenAIRE |
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