Oral administration of yeast β-glucan ameliorates inflammation and intestinal barrier in dextran sodium sulfate-induced acute colitis

被引：67

作者：

Han, Feifei ^{[1
]}

Fan, Hanxue ^{[1
]}

Yao, Ming ^{[1
]}

Yang, Shasha ^{[1
]}

Han, Jianzhong ^{[1
]}

机构：

[1] Zhejiang Gongshang Univ, Sch Food Sci & Biotechnol, Food Safety Key Lab Zhejiang Prov, Hangzhou 310018, Zhejiang, Peoples R China

来源：

JOURNAL OF FUNCTIONAL FOODS | 2017年 / 35卷

关键词：

Inflammation; Intestinal barrier; Tight junction; Colitis; Yeast beta-glucan; ULCERATIVE-COLITIS; CROHNS-DISEASE; INJURY; MICE; INFILTRATION; PERMEABILITY; PATHOGENESIS; DISRUPTION; RESPONSES; CELLS;

D O I：

10.1016/j.jff.2017.05.036

中图分类号：

TS2 [食品工业];

学科分类号：

0832 ;

摘要：

Ulcerative colitis is a chronic inflammatory disease that is characterized by relapsing inflammation and dysfunction within the gastrointestinal tract. The purpose of this study was to investigate the protective effects of yeast beta-glucan on regulating inflammation and disruption of the epithelial barrier in colitis caused by dextran sulfate sodium (DSS). Oral administration of yeast B-glucan reduced clinical symptoms, inflammatory infiltrates and cell apoptosis in the colon epithelium, ameliorated intestinal permeability and the structural integrity of tight junctions. Moreover, treatment with yeast B-glucan not only decreased myeloperoxidase, eosinophil peroxidase and N-acetyl-beta-D-glucosaminidase levels, but also modified the immune status characterized by the change in immunoglobulin levels in DSS-treated mice. These results suggest that yeast beta-glucan improves DSS-induced changes in mucosal inflammatory lesions and the intestinal barrier by inhibiting the expression of inflammatory mediators and enhancing the expression of tight junction proteins associated with intestinal permeability. (C) 2017 Elsevier Ltd. All rights reserved.

引用

页码：115 / 126

页数：12

共 60 条

[1] ZONULA OCCLUDENS (ZO)-I AND ZO-2 - MEMBRANE-ASSOCIATED GUANYLATE KINASE HOMOLOGS (MAGUKS) OF THE TIGHT JUNCTION [J].