Telmisartan decreases inflammation by modulating TNF-a, IL-10, and RANK/RANKL in a rat model of ulcerative colitis

• Autor(a) principal: Silva, Késia Karina de Oliveira Souto
• Data de Publicação: 2015
• Outros Autores: Guerra, Gerlane Coelho Bernardo, Araujo, Aurigena Antunes de, Lira, George A., Melo, Maryanne N., Fernandes, Daline, Silva, Arthur L., Araujo Junior, Raimundo Fernandes de
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UFRN
• Texto Completo: https://repositorio.ufrn.br/handle/123456789/46194
• topic: angiotensin II receptor blockers; antiinflammatory; immunohistochemical; rats

Background: Telmisartan is an antihypertensive angiotensin II receptor blocker. This antihypertensive shows antiinflammatory activity. Purpose: In this study, the antiinflammatory activity of telmisartan was tested in an acetic acid (10%) model of ulcerative colitis (UC) in rats. Methods: Rats were given 1, 3, and 5 mg/kg/day of telmisartan orally for 3 days before induction of UC. The same doses were also administered 2 and 24 h after induction. Rats from the non-colitis and non- treated colitis groups were administered vehicle (saline, 5 ml/kg) orally and another group received sulfasalazine (50 mg/kg/day). Colons tissue was analyzed by macroscopic, by histopathology, by the immunohistochemical examination of RANKL/RANK pathway; by ELISA analysis of the levels of IL-10, TNF-a, myeloperoxidase (MPO) and malonaldehyde (MDA). Results: Telmisartan at 5 mg/kg reduced levels of MPO, MDA, TNF-a and increased of IL-10 (p < 0.05). Additionally, telmisartan reduced macroscopic damage, number of ulcers, and inflammatory and histopathological processes such as neutrophil infiltration, changes in cytoarchitecture, and necrosis. Immunohistochemistry revealed down-regulation of nuclear factor-kappaB receptor/nuclear factor- kappaB ligand (RANK/RANKL) in groups treated with sulfasalazine or telmisartan. Conclusion: Telmisartan exerts beneficial effects in an acetic acid model of colitis in rats. These effects may be due to accelerated termination of the acute inflammatory phase, indicated by decreased TNF-a and increased production of IL-10 and low expression of RANKL and RANK. 2014 Institute of Pharmacology, Polish Academy of Sciences. Published by Elsevier Urban & Partner Sp.