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Protective effects of fermented rice extract on ulcerative colitis induced by dextran sodium sulfate in mice

机译:发酵水稻提取物对小鼠葡聚糖硫酸钠诱导的溃疡性结肠炎的保护作用

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Ulcerative colitis (UC) is a chronic inflammatory bowel disease (IBD), characterized by the gut mucosal ulceration. Growing evidence indicates that dysregulation of immune response to the commensal microbiota involves the pathogenesis of IBD. Previous studies have demonstrated the favorable probiotic effects of fermented rice extracts through triple fermentation with Saccharomyces cerevisiae and Weissella cibaria (FRe). Thus, the therapeutic potential of FRe for UC was examined. Dextran sodium sulfate UC mice model was orally administered distilled water as a control, sulfasalazine, or FRe at 300, 200, and 100?mg/kg, once a day for a week. The UC control exhibited body weight loss, bloody stools, and colonic shortening. However, the FRe, especially at 300?mg/kg, led to a reduction in weight loss, disease activity index scores, and colon weight, and an increase in colorectal length. The histopathological analyses revealed mild changes involved in the colonic crypt and mucosal damages in the FRe groups, along with inhibited inflammation. Indeed, the FRe reduced neutrophil infiltration and production of proinflammatory cytokines (i.e., tumor necrosis factor‐α, interleukin‐6/‐8). This was accompanied by the down‐regulation of nuclear factor‐kappa B. The gene expression responsible for the intestinal barrier integrity (i.e., Zonna occludens‐1/‐2, Claudin‐1, Occludin, Mucin‐1/‐2) was up‐regulated in the FRe groups. In addition, the FRe reduced lipid peroxidation and enhanced antioxidant activity. Interestingly, the microbiota dysbiosis was attenuated in the FRe groups, and the number of beneficial bacteria, Lactobacilli and Bifidobacteria, was increased. It suggests that the FRe potently ameliorate UC as a functional food.
机译:溃疡性结肠炎(UC)是一种慢性炎症性肠病(IBD),其特征在于肠道粘膜溃疡。日益增长的证据表明,对非生物皮炎的免疫应答的失调涉及IBD的发病机制。以前的研究表明,通过用酿酒酵母和Weissella cibaria(Fre),通过三重发酵来证明了发酵米提取物的益生菌作用。因此,检查了UC的FRE的治疗潜力。葡聚糖硫酸钠UC小鼠模型是口服蒸馏水作为对照,磺基碱或FRE在300,200和100μmg/ kg,每天一周一次。 UC控制表现出体重减轻,血腥粪便和结肠缩短。然而,FRE,特别是300?Mg / kg,导致减少体重减轻,疾病活动指数分数和结肠重量,并增加结直肠长度。组织病理学分析揭示了在抑制炎症中的结肠隐窝和粘膜损伤中涉及的轻度变化。实际上,Fre降低了中性粒细胞浸润和促炎细胞因子的产生(即肿瘤坏死因子-α,白细胞介素-6 / -8)。这伴随着核因子-Kappa B的下调。对肠道阻隔完整性的基因表达(即,Zonna occludens-1 / -2,Claudin-1,occludin,粘蛋白-1 / -2)都是Up - 在Fre组中进行。此外,FRE降低脂质过氧化和增强的抗氧化活性。有趣的是,微生物菌脱敏病毒在FRE组中衰减,有益细菌,乳酸杆菌和双歧杆菌的数量增加。它表明,FRE易于改善UC作为功能性食物。

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