title: Polysaccharides from Acanthopanax senticosus enhances intestinal integrity through inhibiting TLR4/NF-κB signaling pathways in lipopolysaccharide-challenged mice.
abstract: 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 E2 (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)-κB p65 (P < 0.05) and its protein expression. These findings suggest that ASPS improves intestinal integrity under inflammation conditions connected with inhibiting TLR4/NF-κB signaling pathways.
authors.affiliation: Institute of Animal Husbandry and Veterinary, Shenyang Agricultural University, Shenyang, China.
authors.forename: Jie
authors.initials: J
authors.lastname: Han
authors.affiliation: Institute of Animal Husbandry and Veterinary, Shenyang Agricultural University, Shenyang, China.
authors.forename: Lixia
authors.initials: L
authors.lastname: Liu
authors.affiliation: Liaoning Academy of Agricultural Sciences, Shenyang, China.
authors.forename: Ning
authors.initials: N
authors.lastname: Yu
authors.affiliation: Institute of Animal Husbandry and Veterinary, Shenyang Agricultural University, Shenyang, China.
authors.forename: Jing
authors.initials: J
authors.lastname: Chen
authors.affiliation: Institute of Animal Husbandry and Veterinary, Shenyang Agricultural University, Shenyang, China.
authors.forename: Baoshan
authors.initials: B
authors.lastname: Liu
authors.affiliation: Institute of Animal Husbandry and Veterinary, Shenyang Agricultural University, Shenyang, China.
authors.forename: Di
authors.initials: D
authors.lastname: Yang
authors.affiliation: Institute of Animal Husbandry and Veterinary, Shenyang Agricultural University, Shenyang, China.
authors.forename: Guoshun
authors.initials: G
authors.lastname: Shen
mesh_terms: D000284:Administration, Oral; D000818:Animals; D016207:Cytokines / Q000378:metabolism; D003864:Depression, Chemical; D028001:Eleutherococcus / Q000737:chemistry*; D004926:Escherichia coli; D007249:Inflammation; D018836:Inflammation Mediators / Q000378:metabolism; D007410:Intestinal Diseases / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism* / Q000473:pathology; D008070:Lipopolysaccharides / Q000009:adverse effects; D008297:Male; D008815:Mice, Inbred Strains; D016328:NF-kappa B / Q000378:metabolism* / Q000502:physiology; D008517:Phytotherapy; D011134:Polysaccharides / Q000008:administration & dosage* / Q000302:isolation & purification / Q000494:pharmacology*; D015398:Signal Transduction / Q000187:drug effects*; D051197:Toll-Like Receptor 4 / Q000378:metabolism* / Q000502:physiology
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators; D008070:Lipopolysaccharides; D016328:NF-kappa B; D011134:Polysaccharides; C493487:Tlr4 protein, mouse; D051197:Toll-Like Receptor 4
keywords: herbal extract; intestinal inflammation; metabolism; pro-inflammatory cytokines; toll-like receptor 4