Effects of aminoguanidine on some biochemical changes associated with acetic acid -induced ulcerative colitis in rats

Inducible nitric oxide has been implicated the pathogenesis associated with ulcerative colitis. Moreover oxidative stress linked with ulcerative colitis is responsible for inactivation of many antioxidants enzymes. The aim of the present study is to investigate the protective effect of aminoguanidine against acetic acid-inducedulcerative colitis in rats. In this study the effects of aminoguanidine1g/l supplementation to the rats on some biochemical markers for oxidative stress were assessed. In addition, the colonic tissues macroscopic and microscopic changes were investigated. The results of present study indicated that intra-rectal inoculation of the rats with 4% acetic acid for 3 consecutive days revealed a significant alteration of macroscopic, microscopic as well as increase of colon weight and decrease colon length. Aminoguanidine administration was significantly ameliorating the degeneration caused by acetic acid inoculation. Pretreatment of rats with aminoguanidinepreserve the activity of serum paraoxonase by about (36%), and colon tissues catalase (144%), moreover aminoguanidine treatment elevate reduced glutathione tissues colon content by 267 % compared with acetic acid administration. Serum nitrate level, colonic tissue content of malondialdehyde and protein carbonyls were reduced by aminoguanidine prior treatment by 175%, 47% and 60 % respectively compared with ulcerative colitis rats. Finally we concluded that increase of nitric oxide plays an important role in the pathogenesis of ulcerative colitis. This resulted in decrease of colonic tissues reduced glutathione contents as well as reduction of some antioxidant enzymes activities. Restoration of nitric oxide level by aminoguanidine treatment is responsible for attenuation of oxidative stress caused by acetic acid administration. Our results suggested that aminoguanidine treatment can reduce the inflammation associated with ulcerative colitis as confirmed with histopathological investigations.