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低分子量硒代氨基多糖对肠道黏膜氧化损伤的保护作用。

Protective Effect of Low Molecular Weight Seleno-Aminopolysaccharide on the Intestinal Mucosal Oxidative Damage.

机构信息

Zhejiang Provincial Engineering Technology Research Center of Marine Biomedical Products, School of Food Science and Pharmaceutics, Zhejiang Ocean University, Zhoushan 316022, China.

Department of Agriculture, Jiaxing Vocational Technical College, Jiaxing 314036, China.

出版信息

Mar Drugs. 2019 Jan 18;17(1):64. doi: 10.3390/md17010064.

DOI:10.3390/md17010064
PMID:30669387
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6356751/
Abstract

Low molecular weight seleno-aminopolysaccharide (LSA) is an organic selenium compound comprising selenium and low molecular weight aminopolysaccharide (LA), a low molecular weight natural linear polysaccharide derived from chitosan. LSA has been found to exert strong pharmacological activity. In this study, we aimed to investigate the protective effect of LSA on intestinal mucosal oxidative stress in a weaning piglet model by detecting the growth performance, intestinal mucosal structure, antioxidant indices, and expression level of intracellular transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) and its related factors. Our results indicated that LSA significantly increased the average daily gain and feed/gain ( < 0.05), suggesting that LSA can effectively promote the growth of weaning piglets. The results of scanning electron microscope (SEM) microscopy showed that LSA effectively reduced intestinal damage, indicating that LSA improved the intestinal stress response and protected the intestinal structure integrity. In addition, diamine oxidase (DAO) and d-lactic acid (d-LA) levels remarkably decreased in LSA group compared with control group ( < 0.05), suggesting that LSA alleviated the damage and permeability of weaning piglets. LSA significantly increased superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and total antioxidant capacity (T-AOC) levels, but decreased malondialdehyde (MDA) level, indicating that LSA significantly enhanced the antioxidant capacity and reduced oxidative stress in weaning piglets. RT-PCR results showed that LSA significantly increased GSH-Px1, GSH-Px2, SOD-1, SOD-2, CAT, Nrf2, HO-1, and NQO1 gene expression ( < 0.05). Western blot analysis revealed that LSA activated the Nrf2 signaling pathway by downregulating the expression of Keap1 and upregulating the expression of Nrf2 to protect intestinal mucosa against oxidative stress. Collectively, LSA reduced intestinal mucosal damage induced by oxidative stress via Nrf2-Keap1 pathway in weaning stress of infants.

摘要

低分子硒-氨基多糖(LSA)是一种有机硒化合物,由硒和低分子氨基多糖(LA)组成,LA 是一种低分子量天然线性多糖,来源于壳聚糖。研究发现 LSA 具有很强的药理活性。本研究旨在通过检测生长性能、肠黏膜结构、抗氧化指标以及细胞内转录因子核因子红细胞 2 相关因子 2(Nrf2)及其相关因子的表达水平,探讨 LSA 对断奶仔猪模型肠黏膜氧化应激的保护作用。结果表明,LSA 显著提高了平均日增重和饲料增重比( < 0.05),说明 LSA 能有效促进断奶仔猪生长。扫描电子显微镜(SEM)结果显示,LSA 能有效减轻肠损伤,表明 LSA 改善了肠应激反应,保护了肠结构的完整性。此外,与对照组相比,LSA 组二胺氧化酶(DAO)和 D-乳酸(d-LA)水平显著降低( < 0.05),表明 LSA 减轻了断奶仔猪的损伤和通透性。LSA 显著提高了超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)和总抗氧化能力(T-AOC)水平,降低了丙二醛(MDA)水平,表明 LSA 显著增强了断奶仔猪的抗氧化能力,减轻了氧化应激。RT-PCR 结果表明,LSA 显著增加了 GSH-Px1、GSH-Px2、SOD-1、SOD-2、CAT、Nrf2、HO-1 和 NQO1 基因的表达( < 0.05)。Western blot 分析表明,LSA 通过下调 Keap1 表达和上调 Nrf2 表达激活了 Nrf2 信号通路,从而保护肠黏膜免受氧化应激。综上所述,LSA 通过 Nrf2-Keap1 通路减轻了氧化应激引起的肠黏膜损伤,在婴幼儿断奶应激中具有保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9d6/6356751/18b92c706e4c/marinedrugs-17-00064-g007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9d6/6356751/18b92c706e4c/marinedrugs-17-00064-g007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9d6/6356751/3dddf6cce69b/marinedrugs-17-00064-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9d6/6356751/18b92c706e4c/marinedrugs-17-00064-g007.jpg

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