Objective: To study the protective eff ects of cinnamic acid on dextran sodium sulfate (DSS) induced ulcerative colitis (UC) in mice. Materials and methods. Forty adult male mice were randomLy divided into fi ve groups, control group, an induction group received 3% DSS in drinking water for 7 consecutive days. Two treatment groups received oral suspension of cinnamic acid 50 and 25 mg/kg, respectively and 3% DSS in drinking water, for 7 consecutive days. The fi nal group received oral suspension of cinnamic acid 50 mg/kg for the latter 7 days without DSS in drinking water. All the animals were euthanized on day eight. The colon of animals was extracted and divided into two sections, the middle was homogenized and biochemically analyzed using the mean levels of total superoxide dismutase (SOD), and malondialdehyde, catalase, the distal for histopathological examination Results: Total SOD, malondialdehyde, and catalase show signifi cant results in the model group when compared to thecontrol group. DSS with cinnamic acid 50 mg/kg group and DSS with cinnamic acid 25 mg/kg revealed a signifi cant (p < 0.05) increase in total SOD and MDA and signifi cant reduction in catalase when compared to the model group. Histopathological examination showed a signifi cant reduction of infl ammatory signs in all cinnamic acid-treated groups compared to the DSS model group. Conclusion: The treatment with cinnamic acid signifi cantly decreased the levels of DSS-associated oxidative stress. This fi nding supports the idea that the use of this substance could be used as a potential therapy for patients with ulcerative colitis.
