Effect of COX-2 inhibitor after TNBS-induced colitis in Wistar rats.
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.
Paiotti
Ana Paula Ribeiro
AP
Department of Pathology, Paulista Medical School, Federal University of Sao Paulo, Rua Botucatu, Sao Paulo, 04023-062, Brazil. a.paiotti@unifesp.br
Miszputen
Sender Jankiel
SJ
Oshima
Celina Tizuko Fujiyama
CT
de Oliveira Costa
Henrique
H
Ribeiro
Daniel Araki
DA
Franco
Marcello
M
D000818:Animals; D052246:Cyclooxygenase 2 Inhibitors / Q000627:therapeutic use*; D004008:Diclofenac / Q000031:analogs & derivatives* / Q000627:therapeutic use; D004195:Disease Models, Animal; D015212:Inflammatory Bowel Diseases / Q000139:chemically induced / Q000188:drug therapy* / Q000473:pathology; D012333:RNA, Messenger / Q000737:chemistry; D051381:Rats; D017208:Rats, Wistar; D014302:Trinitrobenzenesulfonic Acid / Q000494:pharmacology
D052246:Cyclooxygenase 2 Inhibitors; D012333:RNA, Messenger; D004008:Diclofenac; D014302:Trinitrobenzenesulfonic Acid; C473384:lumiracoxib