Therapeutic Effects of Aqueous Infusion of Cotinus coggygria Scop Leaves on Dextran Sulphate Sodium-Induced Ulcerative Colitis in Mice.

Abstract

Objective: To investigate the therapeutic effects of aqueous infusion of Cotinus coggygria Scop. leaves (CCLAI) on the dextran sulphate sodium (DSS)-induced ulcerative colitis (UC) in mice.

Methods: A total of 56 C57BL16J mice were divided into 7 groups, including control, DSS model, CCLAI4, CCLAI6, DSS + CCLAI4, DSS + CCLAI6 and DSS + mesalamine groups (n=8). Induction of UC was conducted by 7-day treatment of 3% DSS in mice. CCLAI in 2 different doses (4% and 6%) or mesalamine (250 mg/kg) was administered to C57BL/6J mice orally for 7 consecutive days. The mice in the control group received only tap water. Clinical parameters, antioxidant and anti-inflammatory activities, and histopathological changes in the colon mucosa were examined. Cell proliferatipn index in colon section was determined by immunonistochemical analysis. Colonic cyclooxygenase (COX)-2 and inducible nitric oxide synthase (iNOS) expression levels were detected by Western blot.

Results: CCLAI treatment inhibited DSS-induced colon shortening and significantly improved the Disease Activity Index score (P<0.05 or P<0.01). We also found a significant decrease in myeloperoxidase levels, oxidative stress parameters, and neutrophil infiltration index in the experimental groups receiving CCLAI compared to the control group (all P<0.01). In addition, it was observed that CCLAI administration for 7 days decreased the proinflammatory cytokines levels including interleukin (IL)-1β, IL-6, interferon-γ, and tumor necrosis factor-α in the colon tissues of mice receiving DSS (P<0.05). Further, CCLAI treatment reduced the COX-2 and iNOS levels with an accompanying decrease in prostaglandin E2 and nitric oxide levels, respectively. Additionally, CCLAI treatment markedly decreased the histological lesion score, which was consistent with the reduction of the pro-inflammatory cytokine levels.

Conclusion: CCLAI treatment significantly improved the DSS-induced UC in mice by diminishing histopathological damage in the colonic mucosa and markedly decreased the inflammatory response through inhibiting the formation of inflammatory cytokines and markers of oxidative stress.