Abstract
Naringin is a kind of multi-source food additive which has been explored broadly for its various biological activities and therapeutic potential. In the present study, the protective effect and mechanism of naringin on dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) in mice were investigated. The results showed that naringin significantly alleviated DSS-induced colitis symptoms, including disease activity index (DAI), colon length shortening, and colon pathological damage. The tissue and serum secretion of inflammatory cytokines, as well as the oxidative stress, were decreased accordingly upon naringin intervention. Naringin also decreased the proteins involved in inflammation and increased the expression of tight junction (TJ) proteins. Moreover, naringin increased the relative abundance of Firmicutes/Bacteroides and reduced the content of Proteobacteria to improve the intestinal flora disorder caused by DSS, which promotes the intestinal health of mice. It was concluded that naringin can significantly ameliorate the pathogenic symptoms of UC through inhibiting inflammatory response and regulating intestinal microbiota, which might be a promising natural therapeutic agent for the dietary treatment of UC and the improvement of intestinal symbiosis.
Highlights
Inflammatory bowel disease (IBD) is characterized as an uncontrollable, nonspecific chronic immune-mediated intestinal inflammation which can be divided into Crohn’s disease (CD) and ulcerative colitis (UC)
As an acknowledged index to evaluate ulcerative colitis, the disease activity index (DAI) scores of the dextran sulfate sodium (DSS) group were dramatically increased (p < 0.01), the scores gradually decreased and UC symptoms alleviated upon naringin treatment in a dosedependent manner (Figure 1B)
A mouse model of ulcerative colitis was established with DSS, which showed that naringin had obvious therapeutic effects on ulcerative colitis
Summary
Inflammatory bowel disease (IBD) is characterized as an uncontrollable, nonspecific chronic immune-mediated intestinal inflammation which can be divided into Crohn’s disease (CD) and ulcerative colitis (UC). A general consensus exists that UC is closely associated with immune system dysfunction, intestinal mucosal injury, and dysbacteriosis in people with congenital susceptibility [4]. In this regard, the increases of inflammatory cytokines and oxidative stress are known as important incentives to the occurrence and development of UC [5]. Compositional and metabolic imbalance in the intestinal microbiota could change the intestinal mucosal permeability, concomitantly with the infiltrations of pathogenic bacteria and toxins, leading to long-term inflammatory stimulation and even canceration of the colon mucosa [9,10]. More studies will be needed to define host–microbial relationships relevant to UC and amenable to therapeutic interventions
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