Effect of COX-2 inhibitor lumiracoxib and the TNF-alpha antagonist etanercept on TNBS-induced colitis in Wistar rats

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dc.contributor.author Ribeiro Paiotti, Ana Paula [UNIFESP]
dc.contributor.author Ribeiro, Daniel Araki [UNIFESP]
dc.contributor.author Silva, Roseane Mendes [UNIFESP]
dc.contributor.author Marchi, Patricia [UNIFESP]
dc.contributor.author Oshima, Celina Tizuko Fujiyama [UNIFESP]
dc.contributor.author Artigiani Neto, Ricardo [UNIFESP]
dc.contributor.author Miszputen, Sender Jankiel [UNIFESP]
dc.contributor.author Franco, Marcello [UNIFESP]
dc.date.accessioned 2016-01-24T14:27:18Z
dc.date.available 2016-01-24T14:27:18Z
dc.date.issued 2012-06-01
dc.identifier http://dx.doi.org/10.1007/s10735-012-9400-8
dc.identifier.citation Journal of Molecular Histology. Dordrecht: Springer, v. 43, n. 3, p. 307-317, 2012.
dc.identifier.issn 1567-2379
dc.identifier.uri http://repositorio.unifesp.br/handle/11600/34942
dc.description.abstract Crohn's disease (CD) is associated with gut barrier dysfunction. Besides the baseline barrier defect, a subgroup of patients also expresses an intestinal barrier hyperresponsiveness to nonsteroidal anti-inflammatory drugs. On the other hand, the anti-tumour necrosis factor alpha (TNF-alpha) treatment has brought benefits to these patients. Thus, this study aimed to evaluate the effect of lumiracoxib, a selective-cyclooxygenase-2 (COX-2) inhibitor, and Etanercept (ETC), a TNF-alpha antagonist on the 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced experimental colitis. A total of 47 Wistar rats were randomized into seven groups, as follows: (1) Sham: sham induced-colitis; (2) TNBS: nontreated induced-colitis; (3) Lumiracoxib control; (4) Lumiracoxib-treated induced-colitis; (5) ETC control; (6) ETC-treated induced-colitis; (7) Lumiracoxib-ETC-treated induced-colitis. Rats from groups 6 and 7 presented significant improvement of macroscopic and histopathological damages in the distal colon. the gene expression of COX-2 mRNA, as well of TNF-alpha mRNA, decreased significantly in groups 6 and 7 compared to the TNBS nontreated and lumiracoxib-treated groups. the treatment only with lumiracoxib did not reduce the inflammation on TNBS-induced experimental colitis. ETC attenuated the damage seen in the colon and reduced the inflammation caused by TNBS. Our results suggest that down-regulation of TNF-alpha and COX-2 resulted in a decrease in inflammation caused by TNBS and thus provided some protection from the colonic damage caused by TNBS. en
dc.description.sponsorship Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorship Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.description.sponsorship Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.format.extent 307-317
dc.language.iso eng
dc.publisher Springer
dc.relation.ispartof Journal of Molecular Histology
dc.rights Acesso restrito
dc.subject Inflammatory bowel disease en
dc.subject TNBS-colitis en
dc.subject TNF-alpha en
dc.subject Cyclooxygenase-2 en
dc.subject Lumiracoxib en
dc.subject Etanercept en
dc.title Effect of COX-2 inhibitor lumiracoxib and the TNF-alpha antagonist etanercept on TNBS-induced colitis in Wistar rats en
dc.type Artigo
dc.rights.license http://www.springer.com/open+access/authors+rights?SGWID=0-176704-12-683201-0
dc.contributor.institution Universidade Federal de São Paulo (UNIFESP)
dc.description.affiliation Universidade Federal de São Paulo, Dept Biosci, UNIFESP, BR-11060001 Santos, SP, Brazil
dc.description.affiliation Universidade Federal de São Paulo, UNIFESP, Dept Pathol, Escola Paulista Med, São Paulo, Brazil
dc.description.affiliation Universidade Federal de São Paulo, Div Gastroenterol, UNIFESP, Escola Paulista Med, BR-11060001 Santos, SP, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Dept Biosci, UNIFESP, BR-11060001 Santos, SP, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo, UNIFESP, Dept Pathol, Escola Paulista Med, São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Div Gastroenterol, UNIFESP, Escola Paulista Med, BR-11060001 Santos, SP, Brazil
dc.identifier.doi 10.1007/s10735-012-9400-8
dc.description.source Web of Science
dc.identifier.wos WOS:000307288800007



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