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- Title
The β<sub>3</sub>-adrenoceptor agonist SR58611A ameliorates experimental colitis in rats.
- Authors
Vasina, V.; Abu-Gharbieh, E.; Barbara, G.; De Giorgio, R.; Colucci, R.; Blandizzi, C.; Bernardini, N.; Croci, T.; Del Tacca, M.; De Ponti, F.
- Abstract
β3-Adrenoceptor agonists protect against experimental gastric ulcers. We investigated the effects of the β3-adrenoceptor agonist SR58611A on 2,4-dinitrobenzene sulphonic acid-induced colitis in rats and analysed the expression of β3-adrenoceptors in the colonic wall. SR58611A was administered orally (1–10 mg kg−1) for 7 days, starting the day before induction of colitis. Colitis was assessed by macroscopic and histological scores, tissue myeloperoxidase activity, interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumour necrosis factor-α (TNF-α) levels. Reverse transcription-polymerase chain reaction and immunohistochemical analysis were used to examine the expression of β3-adrenoceptors. SR58611A significantly reduced the severity of colitis as well as the tissue levels of TNF-α, IL-1β and IL-6. Colitis was associated with a decreased expression of β3-adrenoceptor mRNA in the mucosal/submucosal layer of distal colon and this reduction was not affected by SR58611A. Immunohistochemical analysis revealed β3-adrenoceptors within the muscularis externa, in myenteric neurons and nerve fibres and in the submucosa. β3-Adrenoceptor immunoreactivity was decreased in inflamed tissues compared to controls, particularly in the myenteric plexus; this reduction was counteracted by SR58611A. Amelioration of experimental colitis by the selective β3-adrenoceptor agonist SR58611A suggests that β3-adrenoceptors may represent a therapeutic target in gut inflammation.
- Subjects
BETA adrenoceptors; STOMACH ulcers; DINITROBENZENES; INTERLEUKIN-6; TUMOR necrosis factors; IMMUNOHISTOCHEMISTRY
- Publication
Neurogastroenterology & Motility, 2008, Vol 20, Issue 9, p1030
- ISSN
1350-1925
- Publication type
Article
- DOI
10.1111/j.1365-2982.2008.01138.x