Inflammatory bowel disease (IBD), one kind of intestinal chronic inflammatory disease, is characterized by colonic epithelial barrier injury, overproduction of proinflammatory cytokines, and fewer short-chain fatty acids (SCFAs). The present study is aimed at testing the hypothesis that resistant maltodextrin (RM), a soluble dietary fiber produced by starch debranching, alleviated dextran sulfate sodium- (DSS-) induced colitis in mice. Female C57BL/6 mice with or without oral administration of 50 mg/kg RM for 19 days were challenged with 3% DSS in drinking water to induce colitis (from day 14 to day 19). Although RM could not reverse DSS-induced weight loss or colon shortening, it reduced inflammatory cell infiltration and epithelial damage in colon tissue, as well as the transfer of intestinal permeability indicators including serum diamine oxidase (DAO) and D-lactic acid (D-LA). ELISA analysis indicated that RM significantly suppressed the increase of Th1 cytokines induced by DSS in the colon such as tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ). The levels of proinflammatory cytokines interleukin-1β (IL-1β), IL-17, and IL-8 in the DSS group were significantly higher than those in the control group and RM group, but no significant difference was observed in the RM-DSS group compared with the RM group. Interestingly, IL-10 levels of the DSS group were significantly higher than those of the other groups. With respect to SCFAs, DSS administration significantly decreased the concentration of faecal butyric acid while the RM-DSS group showed a tendency to increase (). In general, RM alleviated dextran sulfate sodium-induced intestinal inflammation through increasing the level of butyric acid and subsequently inhibiting the expression of proinflammatory cytokines.

中文翻译：

---

抗性麦芽糖糊精通过增加丁酸抑制促炎性细胞因子水平，减轻了硫酸葡聚糖钠诱导的肠道炎症损伤。

炎症性肠病（IBD）是一种肠道慢性炎症性疾病，其特征是结肠上皮屏障损伤，促炎性细胞因子的过量产生以及短链脂肪酸（SCFA）较少。本研究旨在检验以下假设：抗性麦芽糊精（RM）是一种通过淀粉脱支产生的可溶性膳食纤维，可减轻小鼠右旋糖酐硫酸钠（DSS-）引起的结肠炎。口服或不口服50 mg / kg RM的雌性C57BL / 6小鼠在19天中用3％DSS的饮用水攻击，以诱发结肠炎（第14天至第19天）。尽管RM不能逆转DSS引起的体重减轻或结肠缩短，但它减少了结肠组织中的炎性细胞浸润和上皮损伤，以及肠通透性指标的转移，包括血清二胺氧化酶（DAO）和D-乳酸（D-LA）。ELISA分析表明，RM能显着抑制DSS诱导的结肠Th1细胞因子的增加，例如肿瘤坏死因子α（TNF- α）和干扰素-γ（IFN- γ）。促炎性细胞因子的水平白细胞介素-1 β（IL-1 β），IL-17，和IL-8的DSS组较对照组和RM组显著较高，但在RM中没有观察到显著差异-DSS组与RM组相比。有趣的是，DSS组的IL-10水平明显高于其他组。就SCFA而言，DSS给药显着降低了粪便丁酸的浓度，而RM-DSS组则显示出增加的趋势（）。通常，RM通过增加丁酸的水平并随后抑制促炎细胞因子的表达来减轻硫酸葡聚糖钠诱导的肠道炎症。