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Activated and inactivated PPARs-γ modulate experimentally induced colitis in rats.

Celinski K, Dworzanski T, Korolczuk A, Slomka M, Radej S, Cichoz-Lach H, Madro A - Med. Sci. Monit. (2011)

Bottom Line: 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.Rosiglitazone inhibits expression of proinflammatory IL-6 and does not affect IL-10.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology, Medical University of Lublin, Lublin, Poland. celinski@mp.pl

ABSTRACT

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.

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Related in: MedlinePlus

Colon homogenate MPO concentrations in the experimental groups.
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f8-medscimonit-17-4-br116: Colon homogenate MPO concentrations in the experimental groups.

Mentions: Anti-inflammatory effects of rosiglitazone were confirmed by MPO determinations in colon homogenates. In group V (receiving TNBS together with rosiglitazone), neutrophil chemotaxis was found to be inhibited, which was reflected by the decreased level of MPO compared to group VI (TNBS). Figure 8 presents the MPO levels in colon homogenates


Activated and inactivated PPARs-γ modulate experimentally induced colitis in rats.

Celinski K, Dworzanski T, Korolczuk A, Slomka M, Radej S, Cichoz-Lach H, Madro A - Med. Sci. Monit. (2011)

Colon homogenate MPO concentrations in the experimental groups.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3539512&req=5

f8-medscimonit-17-4-br116: Colon homogenate MPO concentrations in the experimental groups.
Mentions: Anti-inflammatory effects of rosiglitazone were confirmed by MPO determinations in colon homogenates. In group V (receiving TNBS together with rosiglitazone), neutrophil chemotaxis was found to be inhibited, which was reflected by the decreased level of MPO compared to group VI (TNBS). Figure 8 presents the MPO levels in colon homogenates

Bottom Line: 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.Rosiglitazone inhibits expression of proinflammatory IL-6 and does not affect IL-10.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology, Medical University of Lublin, Lublin, Poland. celinski@mp.pl

ABSTRACT

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.

Show MeSH
Related in: MedlinePlus