Abstract

Inflammatory bowel diseases (IBD), mainly comprising ulcerative colitis and Crohn’s Disease, are complex and multifactorial diseases with unknown etiology. The pathogenesis of IBD is an intricate process that involves epithelial cell damage, excessive immune cell activation and aberrant cytokine response. The dextran sulfate sodium (DSS) induced colitis model is widely used because of its simplicity and many similarities with human ulcerative colitis. This study investigated the protective effects of carvone, a naturally occurring monoterpene with documented anti-inflammatory and antioxidant effects on various organs, on DSS-induced acute colitis. Albino mice utilized in this study were divided into 5 groups: group I served as control group, while mice in group II demonstrated as colitis model obtained by administration of DSS 3% orally for 9 days. Treatment groups include Group III and IV, were mice treated with carvone 50 and 100 mg/kg orally. Mice in group Ⅴ received standard therapy sulfasalazine 100 mg/kg. We reported that carvone 100 mg/kg treatment significantly protected tight junction proteins occludin (348.02±82.04 vs. 114.48±13.34 ng/dl) and ZO-1 (278.43±61.87 vs. 117.38±6.94 ng/dl) compared to non-treated mice. In parallel, mice treated with carvone showed downregulation of inflammatory cytokines TNF-α (2.53±0.20 vs. 6.06±1.67 folds) and IL-6 (1.99±0.44 vs. 5.47±1.65 folds) along with elevation of the anti-inflammatory cytokine IL-10 (90.69±38.73 vs. 28.20±3.51 ng/dl) compared to non-treated animals. In addition, carvone treatment alleviated colitis severity as measured by the disease activity index in terms of body weight loss, stool consistency, and rectal bleeding. Furthermore, histopathological examination revealed that carvone protected colon tissue from the deleterious effect of DSS. In conclusion, carvone protected colon tissue from the damage resulted by DSS- induced acute colitis by preserving tight junction proteins occludin and ZO-1 in parallel with strong anti-inflammatory effects.