Structural Characteristics of Inulin and Microcrystalline Cellulose and Their Effect on Ameliorating Colitis and Altering Colonic Microbiota in Dextran Sodium Sulfate-Induced Colitic Mice

菊粉和微晶纤维素的结构特征及其对改善葡聚糖硫酸钠诱发的结肠炎小鼠结肠炎和改变结肠菌群的影响

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作者:Hanzhen Qiao, Tongxi Zhao, Jie Yin, Yichen Zhang, Hongmei Ran, Shaojie Chen, Ziwei Wu, Ran Zhang, Xingkexin Wang, Liping Gan, Jinrong Wang

Abstract

Several studies have reported that dietary fibers (DFs) from plants may exert beneficial effects on inflammatory bowel disease. In the present study, we investigated the structural differences of soluble DF (inulin) and insoluble DF (microcrystalline cellulose, MCC) and their effects on the intestinal barrier integrity, gut microbiota community, and inflammation response in mice with dextran sodium sulfate (DSS)-induced colitis. Mice were fed for 21 days with diets containing inulin or MCC (2.5 g/kg body weight), and colitis was induced by administration of DSS (4% w/v) in drinking water during the last 8 days of experimentation. The results showed that inulin and MCC differ in morphology and structure. MCC exhibited a smaller particle size, a larger specific surface area, and higher thermal stability than inulin. In addition, both inulin and MCC restored various physical signs (body weight, colon weight and length, disease activity index score, and infiltration of inflammatory cells), gut barrier function (as evidenced by the increased expression of claudin-3, claudin-7, ZO-2, occludin, JAM-2, and MUC-3 and the decreased activity of myeloperoxidase activity), downregulation of mRNA expression of proinflammatory cytokines (caspase-1, NLPR3, TLR4, TNF-α, and IL-1β), and modulation of colon microbiota community. Taken together, the present study demonstrates that DFs differ in morphology and structure and ameliorate DSS-induced colitis in mice by blocking proinflammatory cytokines, reinforcing gut barrier integrity, and modulating gut microbiota. Therefore, DFs, especially inulin, are promising dietary supplements to alleviate intestinal inflammation.

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