Effect of N-acetylcysteine on an experimental model of indomethacin induced inflammatory bowel disease

Abstract

N-acetylcysteine (NAC) is a thiol compound can act both as a precursor of GSH and as a direct ROS scavenger. Moreover, NAC has been purported to have anti-inflammatory properties. The aim of this study was to investigate the effects of NAC on a rat model of inflammatory bowel disease (IBD). Model of IBD was induced by subcutaneous Indomethacin (Indo) at a dose rate of 9 mg/kg for two days at 24 h intervals. NAC in two doses (500mg/Kg, 1 g/kg body weight po) was administrated for seven consecutive days beginning 24 h after the first Indo injection. Body weight loss, small intestine weight / length ratio, macroscopic damage, histological study, as well as by biochemical measurement of reduced glutathione (GSH) and superoxide dismutase (SOD) activity in the small intestine tissue were used for assessment of small intestinal injury. NAC in two doses especially at dose (1g/kg) revealed increase in small intestine weight/length ratio, macroscopic and microscopic small intestinal damage scores caused by administration of indomethacin with no statistical significance comparing with Indo control group (p>0.05). The increased of the oxidative stress was observed in both doses of NAC especially at dose (1g/kg) by decrease the levels of GSH and SOD activity with no statistical significance comparing with Indo control group (p>0.05). The conclusion of this study is NAC didn't enhance intestinal inflammation induced by Indo (rat model of IBD) in both doses, in contrast rising in inflammation and oxidative stress was observed in NAC treated groups especially at dose 1g/kg