The PPARγ Agonist Rosiglitazone Impairs Colonic Inflammation in Mice with Experimental ColitisReportar como inadecuado

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Journal of Clinical Immunology

, Volume 27, Issue 3, pp 275–283

First Online: 14 February 2007Received: 13 November 2006Accepted: 19 January 2007 Various animal models showed that peroxisome proliferator-activated receptor PPARγ agonists, when given as a gavage shortly preceding colitis induction, protect against inflammatory bowel disease IBD. We have examined the effects of 16 days rosiglitazone treatment via the diet prior to dextran sodium sulphate DSS-induced colitis in mice. After 7 days DSS in the drinking water, rosiglitazone-fed mice had lost significantly more weight than control mice. Rosiglitazone-treated mice had more diarrhea, weight of colon and spleen were increased, and length of colon was decreased. Histology showed that rosiglitazone-treated mice had more severe colitis, mainly caused by more ulceration, crypt loss, and edema. Immunofluorescence showed a loss of tight junction structure Zonula Occludens protein 1 ZO-1 in colons of rosiglitazone-treated mice as compared to control mice. Also, serum amyloid P component SAP concentrations in plasma were increased. However, concentrations of tumor necrosis factor TNF-α and interferon IFN-γ in colon homogenates, and TNF-α in spleen homogenates were significantly decreased, whereas interleukin IL-10 in spleen homogenates was increased. Other cytokines IL-2, IL-4, IL-6, IL-12p70 and monocyte chemotactic protein MCP-1 and myeloperoxidase MPO concentrations showed no differences. In conclusion, 16 days pretreatment with rosiglitazone impaired DSS-induced colitis in mice.

KEY WORDSDSS-induced colitis rosiglitazone peroxisome proliferator-activated receptor PPAR  Download fulltext PDF

Autor: Julian D. Ramakers - Marleen I. Verstege - Geertje Thuijls - Anje A. Te Velde - Ronald P. Mensink - Jogchum Plat


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