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糖肽通过调节小鼠肠道微生物群落的组成和多样性来预防急性结肠炎的发生和进展。

Glycopeptide prevents the development and progression of acute colitis by regulating the composition and diversity of the gut microbiota in mice.

机构信息

Beijing Advanced Innovation Centre for Soft Matter Science and Engineering, College of Life Science and Technology, Beijing University of Chemical Technology, Beijing, China.

Institute of Medical Biology, Chinese Academy of Medical Sciences, Peking Union Medical College, Kunming, China.

出版信息

Front Cell Infect Microbiol. 2022 Aug 9;12:921075. doi: 10.3389/fcimb.2022.921075. eCollection 2022.

DOI:10.3389/fcimb.2022.921075
PMID:36017369
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9395742/
Abstract

In most cases, recurrent chronic colitis is caused by the recurrence of acute colitis after incomplete recovery and re-exposure to irritating factors, and the gut microbiome, which is the largest micro-ecosystem in the human body, plays a crucial role in the development of colitis. Plant polysaccharides have always been reported to have the ability for anti-inflammation, and they are closely related to the gut microbiome. Glycopeptide (LbGP), the most potent component obtained by further isolation and purification from fruit, has been shown to inhibit inflammation in animal models. However, its therapeutic efficacy in colitis and its mechanism in gut microbiota regulation have not been fully studied. In our study, the dextran sulfate sodium (DSS)-induced mouse model was used to dynamically evaluate the effect of LbGP in the treatment of acute colitis and the mechanism from the perspective of the gut microbiome through the 16S rDNA sequence. The results showed that LbGP treatment significantly alleviated acute colitis and improved the gut microbiome compared with that in the model group. Harmful bacteria, such as spp. and , were inhibited and probiotics, such as spp., spp., and spp., were increased by LbGP treatment. Further, a Random Forest analysis with 10-fold cross-validation identified a family named representing colitis development and recovery upon LbGP treatment. In conclusion, our study demonstrated the capability of LbGP to prevent the development of acute colitis by regulating the composition and diversity of the gut microbiota and highlighted the dynamic process of gut microbiota with the colitis progression. Further, it provides evidence to develop LbGP as a functional food supplement and future drug acting on intestinal disease.

摘要

在大多数情况下,复发性慢性结肠炎是由急性结肠炎在不完全恢复后复发和再次暴露于刺激性因素引起的,而肠道微生物组是人体最大的微生态系统,在结肠炎的发展中起着至关重要的作用。植物多糖一直被报道具有抗炎能力,它们与肠道微生物组密切相关。从水果中进一步分离和纯化得到的最有效成分糖肽(LbGP)已被证明在动物模型中具有抑制炎症的作用。然而,其在结肠炎中的治疗效果及其对肠道微生物群调节的机制尚未得到充分研究。在我们的研究中,使用葡聚糖硫酸钠(DSS)诱导的小鼠模型,通过 16S rDNA 序列从肠道微生物组的角度动态评估 LbGP 在治疗急性结肠炎中的作用及其机制。结果表明,与模型组相比,LbGP 治疗显著缓解了急性结肠炎并改善了肠道微生物组。LbGP 治疗抑制了有害细菌,如 spp.和 spp.,并增加了益生菌,如 spp.、 spp.和 spp.。此外,使用 10 倍交叉验证的随机森林分析确定了一个名为的家族,代表了 LbGP 治疗后结肠炎的发展和恢复。总之,我们的研究表明 LbGP 通过调节肠道微生物群的组成和多样性来预防急性结肠炎的发生,并强调了肠道微生物群在结肠炎进展过程中的动态变化。此外,它为开发 LbGP 作为功能性食品补充剂和未来治疗肠道疾病的药物提供了证据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3143/9395742/193e5c874b9c/fcimb-12-921075-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3143/9395742/5d7c2b50adbd/fcimb-12-921075-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3143/9395742/767d1db95851/fcimb-12-921075-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3143/9395742/09039eb78472/fcimb-12-921075-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3143/9395742/a2360454c968/fcimb-12-921075-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3143/9395742/f69d1aa7bb2b/fcimb-12-921075-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3143/9395742/1a163d01964b/fcimb-12-921075-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3143/9395742/193e5c874b9c/fcimb-12-921075-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3143/9395742/5d7c2b50adbd/fcimb-12-921075-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3143/9395742/767d1db95851/fcimb-12-921075-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3143/9395742/09039eb78472/fcimb-12-921075-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3143/9395742/a2360454c968/fcimb-12-921075-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3143/9395742/f69d1aa7bb2b/fcimb-12-921075-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3143/9395742/1a163d01964b/fcimb-12-921075-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3143/9395742/193e5c874b9c/fcimb-12-921075-g007.jpg

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