4.7 Article

Polysaccharide of Hericium erinaceus attenuates colitis in C57BL/6 mice via regulation of oxidative stress, inflammation-related signaling pathways and modulating the composition of the gut microbiota

期刊

JOURNAL OF NUTRITIONAL BIOCHEMISTRY
卷 57, 期 -, 页码 67-76

出版社

ELSEVIER SCIENCE INC
DOI: 10.1016/j.jnutbio.2018.03.005

关键词

Inflammatory bowel disease; Anti-inflammatory; Gut dysbiosis; Akkermansia; PICRUSt

资金

  1. National Natural Science Foundation of China [31771514]
  2. national first-class discipline program of Light Industry Technology and Engineering [LITE2018-18]
  3. Industry-Academia Cooperation Innovation Fund Project of Jiangsu Province, China [BY2012052]

向作者/读者索取更多资源

Inflammatory bowel disease (IBD) is a disease caused by a dysregulated immune with unknown etiology. Hericium erinaceus (H. erinaceus) is a Chinese medicinal fungus, with the effect of prevention and treatment of gastrointestinal disorders. In this study, we have tested the anti-inflammatory effect of polysaccharide of H. erinaceus (HECP, Mw: 86.67 kDa) in the model of dextran sulfate sodium (DSS)-induced colitis in C57BL/6 mice. Our data indicated that HECP could improve clinical symptoms and down-regulate key markers of oxidative stresses, including nitric oxide (NO), malondialdehyde (MDA), total superoxide dismutase (T-SOD), and myeloperoxidase (MPO). HECP also suppressed the secretion of interleukin (IL)-6, interleukin (IL)-1 beta, tumor necrosis factor (TNF)-alpha and the expression of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS) and decreased the expression of related mRNA. Meanwhile, HECP blocked phosphorylation of nuclear factor-KB (NF-kB) p65, NF-kB inhibitor alpha (iKB-alpha), mitogen-activated protein kinases (MAPK) and Protein kinase B (Akt) in DSS-treated mice. Moreover, HECP reversed DSS-induced gut dysbiosis and maintained intestinal barrier integrity. In conclusion, HECP ameliorates DSS-induced intestinal injury in mice, which suggests that HECP can serve as a protective dietary nutrient against IBD. (C) 2018 Published by Elsevier Inc.

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