Inhibition of p38 MAP kinase- and RICK/NF-κB-signaling suppresses inflammatory bowel disease EIKE HOLLENBACH * ,† , 1 , MANFRED NEUMANN * , 1 , MICHAEL VIETH ‡ , ALBERT ROESSNER ‡ , PETER MALFERTHEINER † , 2 and MICHAEL NAUMANN * , 2 ,3 * Institute of Experimental Internal Medicine; † Department of Gastroenterology, Hepatology and Infectiology; and ‡ Institute of Pathology Otto-von-Guericke-University, Magdeburg, Germany 3 Correspondence: Institute of Experimental Internal Medicine, Otto-von-Guericke-University, Leipziger Strasse 44, Magdeburg D-39120, Germany. E-mail: naumann@medizin.uni-magdeburg.de <h3>SPECIFIC AIMS</h3> Inhibition of p38-MAPK is therapeutically beneficial for treatment of inflammatory bowel disease (IBD) indicating the importance of p38 for IBD pathogenesis. Using DSS-induced ulcerative colitis as an established mouse model, we pursued the following specific aims: 1) analysis of the effect of SB203580, an inhibitor supposedly specific for p38, on the macroscopic disease activity index (DAI), histological alterations, and the cytokine profile of inflamed tissue; 2) studying the effects of SB203580 on key signaling factors known to be critical for inflammation such as p38 and NF-κB; and 3) identification of new target molecules which may be useful for future therapies of IBD. <h3>PRINCIPAL FINDINGS</h3> <h3>1. SB203580 reduces the disease activity index and the histological disease
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Inhibition of p38 MAP kinase- and RICK/NF-κB-signaling suppresses inflammatory bowel disease
HOLLENBACH, EIKE; NEUMANN, MANFRED; VIETH, MICHAEL; ROESSNER, ALBERT; MALFERTHEINER, PETER; NAUMANN, MICHAEL
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, Volume 18 (13): 1550
Fed of American Socs for Experimental Biology – Oct 1, 2004
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