首页> 美国卫生研究院文献>Asian-Australasian Journal of Animal Sciences >Effect of Polysaccharides from Acanthopanax senticosus on Intestinal Mucosal Barrier of Escherichia coli Lipopolysaccharide Challenged Mice
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Effect of Polysaccharides from Acanthopanax senticosus on Intestinal Mucosal Barrier of Escherichia coli Lipopolysaccharide Challenged Mice

机译:刺五加多糖对大肠杆菌脂多糖攻击小鼠肠道黏膜屏障的影响

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摘要

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 α (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.
机译:为了研究刺五加(ASPS)的多糖在预防脂多糖(LPS)引起的肠损伤中的作用,将18只小鼠(5周龄)分为三组,每组六次重复一只小鼠。通过有或没有ASPS(300mg / kg体重)的口服管饲法给予小鼠14天,并在第15天注射盐水或LPS。攻击后4小时收集肠样品。结果表明,ASPS改善了LPS诱导的LPS攻击小鼠的消化能力下降,这表现为肠道乳糖酶活性的增加(45%,p <0.05),以及肠道形态的改善,绒毛高度的提高(20.84% ,p <0.05)和绒毛高度:隐窝深度比率(42%,p <0.05),空肠隐窝深度较低(15.55%,p <0.05),以及涉及occludin-1的肠紧密连接蛋白表达增强( 71.43%,p <0.05)。 ASPS还可以预防肠道炎症反应,这是由于肠道炎症介质(包括肿瘤坏死因子α(22.28%,p <0.05)和热休克蛋白(HSP70)(77.42%,p <0.05))的减少所致。此外,如杯状细胞(24.89%,p <0.05)和三叶肠肽(17.75%,p <0.05)的增加所表明,ASPS也改善了肠粘液层。最后,ASPS促进了表皮生长因子(100%,p <0.05)及其受体(200%,p <0.05)基因的mRNA表达。这些结果表明ASPS可以防止炎症条件下肠粘膜屏障损伤,这可能与表皮生长因子及其受体的基因mRNA表达上调有关。

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