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

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 5mg/kg/day of telmisartan orally for 3 days before induction of UC. The same doses were also administered 2 and 24h 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 (50mg/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-α, myeloperoxidase (MPO) and malonaldehyde (MDA).

Results: Telmisartan at 5mg/kg reduced levels of MPO, MDA, TNF-α 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-α and increased production of IL-10 and low expression of RANKL and RANK.