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膳食盐通过激活成纤维细胞加剧慢性 TNBS 结肠炎所致的肠道纤维化。

Dietary salt exacerbates intestinal fibrosis in chronic TNBS colitis via fibroblasts activation.

机构信息

Normandie Univ, INSERM Unit 1073, University of Rouen Normandy, Rouen, France.

Institute for Research and Innovation in Biomedicine (IRIB), University of Rouen Normandy, Rouen, France.

出版信息

Sci Rep. 2021 Jul 23;11(1):15055. doi: 10.1038/s41598-021-94280-8.

DOI:10.1038/s41598-021-94280-8
PMID:34301970
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8302708/
Abstract

Intestinal fibrosis is a frequent complication in inflammatory bowel diseases (IBD). It is a challenge to identify environmental factors such as diet that may be driving this risk. Intestinal fibrosis result from accumulation of extracellular matrix (ECM) proteins secreted by myofibroblasts. Factors promoting intestinal fibrosis are unknown, but diet appears to be a critical component in its development. Consumption of salt above nutritional recommendations can exacerbate chronic inflammation. So far, high salt diet (HSD) have not been thoroughly investigated in the context of intestinal fibrosis associated to IBD. In the present study, we analyze the role of dietary salt in TNBS chronic colitis induced in rat, an intestinal fibrosis model, or in human colon fibroblast cells. Here, we have shown that high-salt diet exacerbates undernutrition and promoted ECM-associated proteins in fibroblasts. Taken together, our results suggested that dietary salt can activate intestinal fibroblasts, thereby contributing to exacerbation of intestinal fibrosis. Dietary salt may be considered as a putative environmental factor that drives intestinal fibrosis risk.

摘要

肠道纤维化是炎症性肠病(IBD)的常见并发症。确定饮食等环境因素是否会增加这种风险具有挑战性。肠道纤维化是由肌成纤维细胞分泌的细胞外基质(ECM)蛋白积累引起的。促进肠道纤维化的因素尚不清楚,但饮食似乎是其发展的关键因素。摄入超过营养建议的盐会加重慢性炎症。到目前为止,高盐饮食(HSD)在与 IBD 相关的肠道纤维化的背景下尚未得到彻底研究。在本研究中,我们分析了饮食盐在 TNBS 诱导的大鼠慢性结肠炎中的作用,这是一种肠道纤维化模型,或在人结肠成纤维细胞中。在这里,我们已经表明,高盐饮食会加重营养不良并促进成纤维细胞中与 ECM 相关的蛋白。总之,我们的结果表明,饮食盐可以激活肠道成纤维细胞,从而导致肠道纤维化加重。饮食盐可能被视为一种潜在的环境因素,可增加肠道纤维化的风险。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f40/8302708/62d79aa47cfe/41598_2021_94280_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f40/8302708/62b0a619b763/41598_2021_94280_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f40/8302708/45e213373c6c/41598_2021_94280_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f40/8302708/1d3e2e6c1da5/41598_2021_94280_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f40/8302708/f4fce9403e25/41598_2021_94280_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f40/8302708/62d79aa47cfe/41598_2021_94280_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f40/8302708/62b0a619b763/41598_2021_94280_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f40/8302708/45e213373c6c/41598_2021_94280_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f40/8302708/1d3e2e6c1da5/41598_2021_94280_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f40/8302708/f4fce9403e25/41598_2021_94280_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f40/8302708/62d79aa47cfe/41598_2021_94280_Fig5_HTML.jpg

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