Effect of Pentoxifylline on Experimental-dextran Sulphate Sodium-induced Colitis in Rats

Aims: Ulcerative colitis (UC) is considered as an idiopathic, chronic inflammatory bowel disease (IBD) with multifactorial agents. Tumor necrosis factor-alpha (TNF-α) has been suggested to be one of them. The study was designed to evaluate whether pentoxifylline (PTX), as TNF-α suppressor, has a beneficial effect in rats with dextran sulfate sodium (DSS) induced-colitis.
Study Design: Original research papers.
Place and Duration of Study: In both Anatomy Department, Faculty of Medicine, Menoufia University and Animal medicine & Infectious Diseases Department, Faculty of Veterinary Medicine Sadat City Branch , Menoufia University, Egypt , between April 2009 and August 2010.
Methodology: Fifty adult male rats were divided randomly and equally into: control group, model control group, colitis model group, PTX treated group and recovery group. Induction of colitis was made in colitis model by adding DSS to the drinking water; for three weeks (5% for one week followed by 3% of for two weeks). Rats in both PTX treated and model control groups received pentoxifylline for two weeks after the induction of colitis; by intraperitoneal injection (100 mg/kg/day; 1ml /rat). Colon mucosal inflammation and damage were assessed through; clinical, macroscopic, microscopic, morphometric and molecular assessments.
Results: Rats treated with oral administration of DSS for three weeks developed clinical and macroscopic signs of colitis. Treatment with PTX for two weeks, in the treated group or cessation of DSS for two weeks, in the recovery group relieved the colitis symptoms including: diarrhea, reduction in body weight, shortening and ulceration of the colon and extensive colonic damage. All of these were associated with a significant increase in TNF-α m RNA expression. However, an improvement was more significant among treated animals than that in the recovery one.
Conclusion: Pentoxyfylline seems to be an effective in the treatment of ulcerative colitis for further investigation. Also, the unclear dual role of mast cell in both induction and treatment of the disease should be considered in a further investigation.