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探讨壳寡糖对 DSS 诱导的体内外肠道屏障损伤的影响。

Exploring Effects of Chitosan Oligosaccharides on the DSS-Induced Intestinal Barrier Impairment In Vitro and In Vivo.

机构信息

State Key Laboratory of Biochemical Engineering, Institute of Process Engineering, Chinese Academy of Sciences, Beijing 100190, China.

School of Chemical Engineering, University of Chinese Academy of Sciences, Beijing 100049, China.

出版信息

Molecules. 2021 Apr 11;26(8):2199. doi: 10.3390/molecules26082199.

DOI:10.3390/molecules26082199
PMID:33920375
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8070450/
Abstract

Intestinal barrier dysfunction is an essential pathological change in inflammatory bowel disease (IBD). The mucus layer and the intestinal epithelial tight junction act together to maintain barrier integrity. Studies showed that chitosan oligosaccharide (COS) had a positive effect on gut health, effectively protecting the intestinal barrier in IBD. However, these studies usually focused on its impact on the intestinal epithelial tight junction. The influence of COS on the intestinal mucus layer is still poorly understood. In this study, we explored the effect of COS on intestinal mucus in vitro using human colonic mucus-secreted HT-29 cells. COS relieved DSS (dextran sulfate sodium)-induced mucus defects. Additionally, the structural characteristics of COS greatly influenced this activity. Finally, we evaluated the protective effect of COS on intestinal barrier function in mice with DSS-induced colitis. The results indicated that COS could manipulate intestinal mucus production, which likely contributed to its intestinal protective effects.

摘要

肠道屏障功能障碍是炎症性肠病(IBD)的重要病理变化。黏液层和肠道上皮紧密连接共同维持屏障完整性。研究表明,壳寡糖(COS)对肠道健康有积极作用,可有效保护 IBD 中的肠道屏障。然而,这些研究通常集中在其对肠道上皮紧密连接的影响上,对于 COS 对肠道黏液层的影响知之甚少。本研究采用人结肠黏液分泌 HT-29 细胞体外探讨 COS 对肠道黏液的影响。COS 缓解 DSS(葡聚糖硫酸钠)诱导的黏液缺陷。此外,COS 的结构特征对其活性有很大影响。最后,我们评估了 COS 对 DSS 诱导结肠炎小鼠肠道屏障功能的保护作用。结果表明,COS 可以调节肠道黏液的产生,这可能是其肠道保护作用的机制之一。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/037d/8070450/4357dbc05926/molecules-26-02199-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/037d/8070450/8785d2429179/molecules-26-02199-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/037d/8070450/4808c30bfb2e/molecules-26-02199-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/037d/8070450/112a613d6775/molecules-26-02199-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/037d/8070450/e808559a66b1/molecules-26-02199-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/037d/8070450/2d91ce03eb22/molecules-26-02199-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/037d/8070450/f349d39b251d/molecules-26-02199-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/037d/8070450/4357dbc05926/molecules-26-02199-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/037d/8070450/8785d2429179/molecules-26-02199-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/037d/8070450/4808c30bfb2e/molecules-26-02199-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/037d/8070450/112a613d6775/molecules-26-02199-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/037d/8070450/e808559a66b1/molecules-26-02199-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/037d/8070450/2d91ce03eb22/molecules-26-02199-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/037d/8070450/f349d39b251d/molecules-26-02199-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/037d/8070450/4357dbc05926/molecules-26-02199-g007.jpg

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