Effect of COX-2 inhibitor after TNBS-induced colitis in wistar rats

• Published in: Journal of molecular histology Vol. 40; no. 4; pp. 317 - 324
• Main Authors: Paiotti, Ana Paula Ribeiro, Miszputen, Sender Jankiel, Oshima, Celina Tizuko Fujiyama, de Oliveira Costa, Henrique, Ribeiro, Daniel Araki, Franco, Marcello
• Format: Journal Article
• Language: English
• Published: Dordrecht Dordrecht : Springer Netherlands 01.08.2009; Springer Netherlands; Springer Nature B.V
• Subjects: Animals; Biomedical and Life Sciences; Biomedicine; Cell Biology; Cyclooxygenase 2 Inhibitors - therapeutic use; Developmental Biology; Diclofenac - analogs & derivatives; Diclofenac - therapeutic use; Disease Models, Animal; Inflammatory Bowel Diseases - chemically induced; Inflammatory Bowel Diseases - drug therapy; Inflammatory Bowel Diseases - pathology; Life Sciences; Original Paper; Rats; Rats, Wistar; RNA, Messenger - chemistry; Trinitrobenzenesulfonic Acid - pharmacology; Inflammatory bowel disease; TNBS-colitis; Lumiracoxib; Cyclooxygenase-2; qRT-PCR
• ISSN: 1567-2379; 1567-2387; 1567-2387
• DOI: 10.1007/s10735-009-9243-0

Inflammatory bowel disease (IBD) is a common chronic gastrointestinal disorder characterized by alternating periods of remission and active intestinal inflammation. Some studies suggest that antiinflammatory drugs are a promising alternative for treatment of the disease. Thus, this study aimed to evaluate the effect of lumiracoxib, a selective-cyclooxygenase-2 (COX-2) inhibitor, on 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced experimental colitis. Wistar rats (n = 25) were randomized into four groups, as follows: Group (1) Sham group: sham induced-colitis rats; Group (2) TNBS group: nontreated induced-colitis rats; Group (3) Lumiracoxib control group; and Group (4) Lumiracoxib-treated induced-colitis rats. Our results showed that rats from groups 2 and 4 presented similar histopathological damage and macroscopic injury in the distal colon as depicted by significant statistically differences (P < 0.01; P < 0.05) compared to the other two groups. Weak expression of COX-2 mRNA was detected in normal colon cells, while higher levels of COX-2 mRNA were detected in group 2 and group 4. Therapy with lumiracoxib reduced COX-2 expression by 20-30%, but it was still higher and statistically significant compared to data obtained from the lumiracoxib control group. Treatment with the selective COX-2 inhibitor lumiracoxib did not reduce inflammation-associated colonic injury in TNBS-induced experimental colitis. Thus, the use of COX-2 inhibitors for treating IBD should be considered with caution and warrants further experimental investigation to elucidate their applicability.