Manipulation of the l-arginine-nitric oxide pathway in experimental colitis

Publisher Website
Google Scholar
Abstract
The role of the l-arginine-nitric oxide pathway in the pathogenesis of colonic inflammation was assessed using l-arginine and its competitive analogue Nω-nitro-l-arginine methyl ester (l-NAME) in a rat model of colitis. In the first study oral l-arginine 2 per cent (control: 3.4 per cent l-glycine) was administered with and without l-NAME 100 mg/l. Orally administered l-arginine increased colonic inflammation (P = 0.004) and decreased thymic weight (P = 0.0007). Addition of l-NAME reduced the colonic inflammation and prevented loss of body-weight (P < 0.04). In the second study l-NAME was administered orally in concentrations of 100, 200 and 500 mg/l (control: no l-NAME). l-NAME 500 mg/l reduced colonic inflammation and increased thymic weight and body-weight (P < 0.01). Thymic weight and body-weight correlated positively with the concentration of l-NAME administered orally (rs≥0.3, P = 0.04). l-NAME l g/l was administered topically as an enema (control: suspension agent). Topical l-NAME reduced colonic inflammation and increased thymic weight (P < 0.05). These results suggest that the l-arginine-nitric oxide pathway mediates colonic inflammation in this model.
Funding Information
  • Royal College of Surgeons of Edinburgh
  • Department of Health and Social Services