Effect of lecithin on oxidative stress in an experimental model of rats colitis induced by acetic acid

• Autor(a) principal: Colares,Josieli Raskopf
• Data de Publicação: 2016
• Outros Autores: Schemitt,Elizângela Gonçalves, Hartmann,Renata Minuzzo, Moura,Rosa Maria, Morgan-Martins,Maria Isabel, Fillmann,Henrique Sarubbi, Fillmann,Lúcio, Marroni,Norma Possa
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Journal of Coloproctology (Rio de Janeiro. Online)
• Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S2237-93632016000200097
• topic: Ulcerative colitis; Inflammatory bowel disease; Lecithin; Oxidative stress

Abstract Ulcerative colitis (UC) is an inflammatory disease that affects the bowels. Reactive oxygen species (ROS) are involved in the progress of UC. Objective Evaluate the antioxidant effect of lecithin in an experimental model of acute UC induced by administration of acetic acid (AA) in rats. Methods Lecithin (0.5 mL/kg/day) administered orally 2 days before and after induction of colitis with 4% AA in a volume of 4 mL. Twenty-five male Wistar rats were divided in 5 groups: control (CO); control + lecithin (CO + LE); colitis (CL); colitis + lecithin (CL + LE); lecithin + colitis (LE + CL). Anal sphincter pressure, LPO (TBARS), and antioxidant activity of enzymes superoxide dismutase (SOD) and catalase (CAT) were measured, and a histological analysis with H&E was performed. Results and discussion Anal sphincter pressure was significantly smaller in the CO group, lecithin treatment increased it in pre- and post-treated groups. LPO and SOD activity were increased in the CO group and decreased in the lecithin-treated groups. CAT activity was increased in CO group and decreased in lecithin groups. The histological analysis showed damage to the bowels with destruction of crypts, edema, and inflammatory infiltrate. Use of lecithin preserved the crypts and decreased the edema. Conclusion Ulcerative colitis increased lipid peroxidation, and the use of lecithin was effective reducing damage to the bowels in the model of experimental colitis.