Comparative treatment of induced ulcerative colitis in male rat model by using cinnarizine and sulfasalazine

• Main Authors: Rana Kh. Atarbashe, Ahmed Abu-Raghif
• Format: Article
• Language: Arabic
• Published: University of Mosul, College of Veterinary Medicine 2020-05-01
• Series: Iraqi Journal of Veterinary Sciences
• Subjects: cinnarizine; ulcerative colitis; acetic acid; oxidative stress; adhesion molecules
• Online Access: https://vetmedmosul.com/article_164787_04b06cac9d9d998e76113cb52b8ded15.pdf

Ulcerative colitis is a chronic and intermittent illness. The current treatment failed to cure the disease which requires to investigate other drug with minimal side effects. The goal of the research is to assess the histological outcome, antioxidant and anti-inflammatory effects of cinnarizine in comparison with that of sulfasalazine (salazosulfapyridine) in experimentally induced colitis in rats. Acetic acid 4% (vol/vol) was used rectally to induce experimental colitis in rats. After induction, rats were administered either sulfasalazine 100mg/kg or cinnarizine 20 mg/kg as a therapeutic dose in rats orally for one week. The duration of treatment was depended on previous studies. There were estimation of histopathological and clinical parameters also the expression of cytokines (tumor necrosis factor alpha (TNF-α) and interleukin-4 (IL-4)), oxidative stress markers (malondialdehyde (MDA) and myeloperoxidase (MPO)), and adhesion molecules (intercellular adhesion molecule-1 (ICAM-1) and endothelial (E)-Selectin) in the colonic tissue. Results showed that both cinnarizine and sulfasalazine significantly reduced the clinical and histological injury in colon that induced by acetic acid. In addition to the down regulation of the increased colonic cytokines, MDA, MPO parameters and adhesive molecules. These results concluded that cinnarizine had an effective therapeutic role which is comparable with sulfasalazine on the experimental colitis through anti-inflammatory and antioxidant actions with down regulation the colonic adhesion molecule.