Sulfation modification enhances the intestinal regulation of Cyclocarya paliurus polysaccharides in cyclophosphamide-treated mice via restoring intestinal mucosal barrier function and modulating gut microbiota

2021 ◽  
Author(s):  
Yue Yu ◽  
Haibin Zhu ◽  
Mingyue Shen ◽  
Qiang Yu ◽  
Yi Chen ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Intestinal Microbiota ◽  
Barrier Function ◽  
Intestinal Barrier ◽  
Mucosal Barrier ◽  
Intestinal Mucosal Barrier ◽  
Cyclocarya Paliurus ◽  
Mucosal Barrier Function ◽  
Sulfated Derivative

This work aimed to investigate the effects of a sulfated derivative of Cyclocarya paliurus polysaccharide (SCP3) on cyclophosphamide (CTX)-induced intestinal barrier damage and intestinal microbiota in mice.

scholarly journals Fecal Microbiota Transplantation Protects the Intestinal Mucosal Barrier by Reconstructing the Gut Microbiota in a Murine Model of Sepsis

2021 ◽  
Vol 11 ◽  
Author(s):  
Xiaowei Gai ◽  
Huawei Wang ◽  
Yaqing Li ◽  
Haotian Zhao ◽  
Cong He ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Gut Microbiota ◽  
Murine Model ◽  
Barrier Function ◽  
Fecal Microbiota Transplantation ◽  
Fecal Microbiota ◽  
Mucosal Barrier ◽  
Gut Flora ◽  
Intestinal Mucosal Barrier ◽  
Mucosal Barrier Function

The gastrointestinal (GI) tract has long been hypothesized to play an integral role in the pathophysiology of sepsis, and gut microbiota (GM) dysbiosis may be the key factor. Previous studies have shown that the gut flora was significantly altered in critically ill patients. This study aimed to observe what kind of GM dysbiosis is in the early stage of sepsis and whether the application of fecal microbiota transplantation (FMT) can reconstruct the GM of septic mice and restore its protective function on the intestinal mucosal barrier. The study investigated the effect of FMT on gut microbiota, mucosal barrier function, inflammatory response, and survival in a murine model of sepsis established by cecal ligation and puncture (CLP). It is found that FMT can not only reduce morbidity and mortality and restore the abundance and diversity of the gut flora in septic mice, but can also improve the intestinal barrier function by reducing epithelial cell apoptosis, improving the composition of the mucus layer, upregulating the expression of tight junction proteins, and reducing intestinal permeability and the inflammatory response. After FMT, Lachnospiraceae contributed the most to intestinal protection through enhancement of the L-lysine fermentation pathway. FMT offers a microbe-mediated survival advantage in a murine model of sepsis. Therefore, an improved understanding of the connection between microbiota, and systemic illness may yield new therapeutic strategies for patients with sepsis.

scholarly journals Chitosan Ameliorates DSS-Induced Ulcerative Colitis Mice by Enhancing Intestinal Barrier Function and Improving Microflora

2019 ◽  
Vol 20 (22) ◽  
pp. 5751 ◽  
Author(s):  
Jia Wang ◽  
Cuili Zhang ◽  
Chunmei Guo ◽  
Xinli Li
Keyword(s):  
Barrier Function ◽  
Intestinal Microflora ◽  
Intestinal Barrier ◽  
Mucosal Barrier ◽  
Intestinal Barrier Function ◽  
Tight Junction Proteins ◽  
Intestinal Mucosal Barrier ◽  
Tnf Α ◽  
Mucosal Barrier Function ◽  
Junction Proteins

Ulcerative colitis (UC) has been identified as one of the inflammatory diseases. Intestinal mucosal barrier function and microflora play major roles in UC. Modified-chitosan products have been consumed as effective and safe drugs to treat UC. The present work aimed to investigate the effect of chitosan (CS) on intestinal microflora and intestinal barrier function in dextran sulfate sodium (DSS)-induced UC mice and to explore the underlying mechanisms. KM (Kunming) mice received water/CS (250, 150 mg/kg) for 5 days, and then received 3% DSS for 5 days to induce UC. Subsequently, CS (250, 150 mg/kg) was administered daily for 5 days. Clinical signs, body weight, colon length, and histological changes were recorded. Alterations of intestinal microflora were analyzed by PCR-DGGE, expressions of TNF-α and tight junction proteins were detected by Western blotting. CS showed a significant effect against UC by the increased body weight and colon length, decreased DAI (disease activity index) and histological injury scores, and alleviated histopathological changes. CS reduced the expression of TNF-α, promoted the expressions of tight junction proteins such as claudin-1, occludin, and ZO-1 to maintain the intestinal mucosal barrier function for attenuating UC in mice. Furthermore, Parabacteroides, Blautia, Lactobacillus, and Prevotella were dominant organisms in the intestinal tract. Blautia and Lactobacillus decreased with DSS treatment, but increased obviously with CS treatment. This is the first time that the effect of original CS against UC in mice has been reported and it is through promoting dominant intestinal microflora such as Blautia, mitigating intestinal microflora dysbiosis, and regulating the expressions of TNF-α, claudin-1, occludin, and ZO-1. CS can be developed as an effective food and health care product for the prevention and treatment of UC.

Glucagon-Like Peptide-2 Improve Intestinal Mucosal Barrier Function in Aged Rats

2018 ◽  
Vol 22 (6) ◽  
pp. 731-738 ◽  
Author(s):  
Weiying Ren ◽  
Jiayu Wu ◽  
Li Li ◽  
Y. Lu ◽  
Y. Shao ◽  
...  
Keyword(s):  
Barrier Function ◽  
Mucosal Barrier ◽  
Aged Rats ◽  
Intestinal Mucosal Barrier ◽  
Mucosal Barrier Function ◽  
Glucagon Like Peptide
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