Department of Pathology, Paulista Medical School, Federal University of Sao Paulo, Rua Botucatu, Sao Paulo, 04023-062, Brazil.
J Mol Histol. 2009 Aug;40(4):317-24. doi: 10.1007/s10735-009-9243-0. Epub 2009 Nov 22.
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.
炎症性肠病(IBD)是一种常见的慢性胃肠道疾病,其特征是缓解期和活跃的肠道炎症期交替出现。一些研究表明,抗炎药是治疗这种疾病的一种有前途的替代方法。因此,本研究旨在评估选择性环氧化酶-2(COX-2)抑制剂鲁米昔布对 2,4,6-三硝基苯磺酸(TNBS)诱导的实验性结肠炎的影响。Wistar 大鼠(n = 25)随机分为四组:第 1 组(Sham 组):假诱导结肠炎大鼠;第 2 组(TNBS 组):未经治疗的诱导结肠炎大鼠;第 3 组(鲁米昔布对照组);第 4 组(鲁米昔布治疗诱导结肠炎大鼠)。我们的结果表明,与其他两组相比,第 2 组和第 4 组的大鼠在远端结肠的组织病理学损伤和大体损伤相似,差异具有统计学意义(P < 0.01;P < 0.05)。在正常结肠细胞中检测到 COX-2 mRNA 的弱表达,而在第 2 组和第 4 组中检测到更高水平的 COX-2 mRNA。鲁米昔布治疗降低了 COX-2 表达 20-30%,但与鲁米昔布对照组相比仍较高且具有统计学意义。选择性 COX-2 抑制剂鲁米昔布治疗不能减轻 TNBS 诱导的实验性结肠炎相关的结肠炎症损伤。因此,应谨慎考虑使用 COX-2 抑制剂治疗 IBD,并需要进一步的实验研究来阐明其适用性。