首页> 美国卫生研究院文献>International Journal of Molecular Sciences >Eckol Alleviates Intestinal Dysfunction during Suckling-to-Weaning Transition via Modulation of PDX1 and HBEGF
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Eckol Alleviates Intestinal Dysfunction during Suckling-to-Weaning Transition via Modulation of PDX1 and HBEGF

机译:Eckol通过调节PDX1和HBEGF减轻乳头到断奶过渡期间的肠道功能障碍

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摘要

Maintaining intestinal health in livestock is critical during the weaning period. The precise mechanisms of intestinal dysfunction during this period are not fully understood, although these can be alleviated by phlorotannins, including eckol. This question was addressed by evaluating the changes in gene expression and intestinal function after eckol treatment during suckling-to-weaning transition. The biological roles of differentially expressed genes (DEGs) in intestinal development were investigated by assessing intestinal wound healing and barrier functions, as well as the associated signaling pathways and oxidative stress levels. We identified 890 DEGs in the intestine, whose expression was altered by eckol treatment, including pancreatic and duodenal homeobox (PDX)1, which directly regulate heparin-binding epidermal growth factor-like growth factor (HBEGF) expression in order to preserve intestinal barrier functions and promote wound healing through phosphoinositide 3-kinase (PI3K)/AKT and P38 signaling. Additionally, eckol alleviated H O -induced oxidative stress through PI3K/AKT, P38, and 5’-AMP-activated protein kinase (AMPK) signaling, improved growth, and reduced oxidative stress and intestinal permeability in pigs during the weaning period. Eckol modulates intestinal barrier functions, wound healing, and oxidative stress through PDX/HBEGF, and improves growth during the suckling-to-weaning transition. These findings suggest that eckol can be used as a feed supplement in order to preserve the intestinal functions in pigs and other livestock during this process.
机译:在断奶期间,保持牲畜肠道健康至关重要。尽管在这期间,可通过phrotrotannins(包括eckol)缓解肠道功能障碍的确切机制,但尚未完全了解。通过评估在从乳汁到断奶的过渡期进行eckol处理后基因表达和肠功能的变化,可以解决该问题。通过评估肠伤口愈合和屏障功能以及相关的信号传导途径和氧化应激水平,研究了差异表达基因(DEG)在肠道发育中的生物学作用。我们在肠中鉴定出890个DEG,它们的表达被eckol处理所改变,包括胰腺和十二指肠同源盒(PDX)1,它们直接调节肝素结合表皮生长因子样生长因子(HBEGF)的表达,以保留肠道屏障功能通过磷酸肌醇3激酶(PI3K)/ AKT和P38信号传导促进伤口愈合。此外,eckol通过PI3K / AKT,P38和5'-AMP激活的蛋白激酶(AMPK)信号传导减轻了H O诱导的氧化应激,改善了仔猪断奶期间的生长,并降低了氧化应激和肠道通透性。 Eckol通过PDX / HBEGF调节肠道屏障功能,伤口愈合和氧化应激,并在从乳到断奶的过渡过程中改善生长。这些发现表明,eckol可以用作饲料补充品,以在此过程中保持猪和其他牲畜的肠道功能。

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