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Polysaccharides from Acanthopanax senticosus enhances intestinal integrity through inhibiting TLR4/NF‐ κ B signaling pathways in lipopolysaccharide‐challenged mice
Author(s) -
Han Jie,
Liu Lixia,
Yu Ning,
Chen Jing,
Liu Baoshan,
Yang Di,
Shen Guoshun
Publication year - 2016
Publication title -
animal science journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.606
H-Index - 38
eISSN - 1740-0929
pISSN - 1344-3941
DOI - 10.1111/asj.12528
Subject(s) - tlr4 , diamine oxidase , lipopolysaccharide , occludin , tumor necrosis factor alpha , endocrinology , receptor , crypt , medicine , chemistry , signal transduction , inflammation , cytokine , nf κb , tight junction , biology , biochemistry , enzyme
To investigate the role of polysaccharide from Acanthopanax senticosus (ASPS) on lipopolysaccharide (LPS)‐induced intestinal injury, mice in three treatments were administrated orally with or without ASPS (300 mg/kg body weight) for 14 days, followed by challenge with LPS or saline. At 4 h post‐injection, blood and intestinal samples of six mice / treatment were collected. The results showed ASPS ameliorated LPS‐induced intestinal morphological deterioration, proven by improved villus height ( P < 0.05) and villus height : crypt depth ratio ( P < 0.05). ASPS also elevated the mucosal barrier of LPS‐challenged mice, supported by reduced plasma diamine oxidase (DAO) activity ( P < 0.05) and L‐lactate ( P < 0.05), increased mucosal DAO activity ( P < 0.05) as well as enhanced intestinal tight junction proteins expression involving occludin‐1 ( P < 0.05) and zonula occludens‐1 ( P < 0.05). In addition, ASPS decreased LPS‐induced secretion of inflammatory mediators, including tumor necrosis factor (TNF)‐α ( P < 0.05) and prostaglandin E 2 ( P < 0.05). Also, ASPS down‐regulated messenger RNA expression of toll‐like receptor 4 (TLR4) and its downstream signals, including myeloid differentiation factor 88 ( P < 0.05), TNF‐α receptor‐associated factor 6 ( P < 0.05), as well as nuclear factor (NF)‐ κ B p65 ( P < 0.05) and its protein expression. These findings suggest that ASPS improves intestinal integrity under inflammation conditions connected with inhibiting TLR4/NF‐ κ B signaling pathways.