+44 330 818 7254Azza H. El-Medany , Aida A. Guemei, Hanan H. Hagar , Jamila H.El-Medany, Azza M Baraka.
Accumulating data suggest the involvement of renin angiotensin system (RAS) in the pathogenesis of inflammatory bowel disease. The aim of the present study was to evaluate the potential protective and therapeutic effects of captopril and valsartan on acetic acid induced- ulcerative colitis in rats. The results were assessed by macroscopic and microscopic examinations of colonic tissues as ell as by biochemical measurement of malondialdehyde (MDA), tumor necrosis factor alpha (TNF-α), transforming growth factor- beta1 (TGF-b1), angiotensin converting enzyme (ACE), reduced glutathione (GSH) and platelet activating factor (PAF) levels in colonic tissues. Oral treatment with captopril or valsartan in a dose of 30 mg kg-1 body weight, starting one day before induction of colitis and continuing for 1 week (prophylactic groups) or starting one week after induction of colitis and continuing for another one week (therapeutic groups), significantly reduced MDA, TNF-α, PAF, TGF-b1 and significantly increased colonic GSH in colonic tissues as compared to acetic acid control groups. Captopril and valsartan attenuated the macroscopic and microscopic colonic damage induced by acetic acid. No significant difference between the effect of either drug could be detected other than the significant decrease in ACE activity in colonic tissue exerted by captopril and not by valsartan, These results suggest that either captopril or valsartan may be effective in prophylaxis as well as in treatment of ulcerative colitis through targeting RAS.
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