Protective Effect of Naringin on DSS-Induced Ulcerative Colitis in Mice

Peroxisome proliferator-activated receptor gamma (PPAR gamma) is an important member of the nuclear receptor superfamily. Previous studies have shown the satisfactory anti-inflammatory role of PPAR gamma in experimental colitis models, mainly through negatively regulating several transcription factors such as nuclear factor-kappa B (NF-kappa B). Therefore, regulating PPAR gamma and PPAR gamma-related pathways has great promise for treating ulcerative colitis (UC). In the present study, our objective was to explore the potential effect of naringin on dextran sulfate sodium (DSS) induced UC in mice and its involved potential mechanism. We found that naringin significantly relieved DSS-induced disease activities index (DAI), colon length shortening, and colonic pathological damage. Exploration of the potential mechanisms demonstrated that naringin significantly activated DSS-induced PPAR gamma and subsequently suppressed NF-kappa B activation. PPAR gamma inhibitor GW9662 largely abrogated the roles of naringin in vitro. Moreover, DSS induced the activation of mitogen-activated protein kinase (MAPK) and (NOD)-like receptor family pyrin domain containing 3 (NLRP3) inflammasome was inhibited by naringin. Tight junction (TJ) architecture in naringin groups was also maintained by regulating zonula occludens-1 (ZO-1) expression. These results suggested that naringin may be a potential natural agent for protecting mice from DSS-induced UC.