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http://dx.doi.org/10.5713/ajas.15.0534

Effect of Polysaccharides from Acanthopanax senticosus on Intestinal Mucosal Barrier of Escherichia coli Lipopolysaccharide Challenged Mice  

Han, Jie (Institute of Animal Husbandry and Veterinary, Shenyang Agricultural University)
Xu, Yunhe (College of Animal Husbandry and Veterinary, Liaoning Medical University)
Yang, Di (Institute of Animal Husbandry and Veterinary, Shenyang Agricultural University)
Yu, Ning (Institute of Biotechnology Research, Liaoning Academy of Agricultural Sciences)
Bai, Zishan (Institute of Animal Husbandry and Veterinary, Shenyang Agricultural University)
Bian, Lianquan (Institute of Animal Husbandry and Veterinary, Shenyang Agricultural University)
Publication Information
Asian-Australasian Journal of Animal Sciences / v.29, no.1, 2016 , pp. 134-141 More about this Journal
Abstract
To investigate the role of polysaccharide from Acanthopanax senticosus (ASPS) in preventing lipopolysaccharide (LPS)-induced intestinal injury, 18 mice (at 5 wk of age) were assigned to three groups with 6 replicates of one mouse each. Mice were administrated by oral gavage with or without ASPS (300 mg/kg body weight) for 14 days and were injected with saline or LPS at 15 days. Intestinal samples were collected at 4 h post-challenge. The results showed that ASPS ameliorated LPS-induced deterioration of digestive ability of LPS-challenged mice, indicated by an increase in intestinal lactase activity (45%, p<0.05), and the intestinal morphology, as proved by improved villus height (20.84%, p<0.05) and villus height:crypt depth ratio (42%, p<0.05), and lower crypt depth in jejunum (15.55%, p<0.05), as well as enhanced intestinal tight junction proteins expression involving occludin-1 (71.43%, p<0.05). ASPS also prevented intestinal inflammation response, supported by decrease in intestinal inflammatory mediators including tumor necrosis factor ${\alpha}$ (22.28%, p<0.05) and heat shock protein (HSP70) (77.42%, p<0.05). In addition, intestinal mucus layers were also improved by ASPS, as indicated by the increase in number of goblet cells (24.89%, p<0.05) and intestinal trefoil peptide (17.75%, p<0.05). Finally, ASPS facilitated mRNA expression of epidermal growth factor (100%, p<0.05) and its receptor (200%, p<0.05) gene. These results indicate that ASPS can prevent intestinal mucosal barrier injury under inflammatory conditions, which may be associated with up-regulating gene mRNA expression of epidermal growth factor and its receptor.
Keywords
Herbal Extract; Intestinal Barrier; Inflammation; Epidermal Growth Factor; Pro-inflammatory Cytokines; Metabolism;
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