Resveratrol abrogates adhesion molecules and protects against TNBS-induced ulcerative colitis in rats.
Resveratrol, a polyphenol compound with anti-inflammatory properties, has been previously evaluated for its beneficial effects in several ulcerative colitis models. However, the current study elucidates the effect of resveratrol on adhesion molecules, as well as its antioxidant efficacy in a trinitrobenzene sulfonic acid (TNBS)-induced ulcerative-colitis model. Colitis was induced by rectal instillation of TNBS, followed by daily per os  administration of either sulphasalazine (300 mg/kg) or resveratrol (2 and 10 mg/kg) for 7 days. Administration of resveratrol decreased the ulcerative area and colon mass index; these effects were further supported by the reduction in colon inflammation grades, as well as histolopathological changes, and reflected by the stalling of body mass loss. The anti-inflammatory effects of resveratrol were indicated by lowered myeloperoxidase activity, and by suppressing ICAM-1 and VCAM-1 levels in the colon and serum. In addition, it restored a reduced colonic nitric oxide level and reinstated its redox balance, as evidenced by the suppression of lipid peroxides and prevention of glutathione depletion. The anti-ulcerative effect of the higher dose of resveratrol was comparable with those of sulphasalazine. The study confirms the anti-ulcerative effect of resveratrol in TNBS-induced experimental colitis via reduction of neutrophil infiltration, inhibition of adhesive molecules, and restoration of the nitric oxide level, as well as the redox status.
Department of Pharmacology and Toxicology, Cairo University, Egypt.
Dalaal M
DM
Abdallah
Naglaa R
NR
Ismael
D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D001835:Body Weight / Q000187:drug effects; D015815:Cell Adhesion Molecules / Q000037:antagonists & inhibitors*; D003093:Colitis, Ulcerative / Q000139:chemically induced / Q000188:drug therapy* / Q000473:pathology; D003106:Colon / Q000187:drug effects* / Q000473:pathology; D004305:Dose-Response Relationship, Drug; D004353:Drug Evaluation, Preclinical; D005978:Glutathione / Q000032:analysis / Q000187:drug effects; D007249:Inflammation / Q000139:chemically induced / Q000473:pathology*; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood / Q000187:drug effects / Q000502:physiology; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D009195:Peroxidase / Q000032:analysis / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D000077185:Resveratrol; D013267:Stilbenes / Q000494:pharmacology*; D012460:Sulfasalazine / Q000494:pharmacology*; D014302:Trinitrobenzenesulfonic Acid / Q000633:toxicity; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood / Q000187:drug effects / Q000502:physiology
D000894:Anti-Inflammatory Agents, Non-Steroidal; D015815:Cell Adhesion Molecules; D013267:Stilbenes; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D012460:Sulfasalazine; D014302:Trinitrobenzenesulfonic Acid; D009195:Peroxidase; D005978:Glutathione; D000077185:Resveratrol