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NOD样受体介导肠道上皮稳态屏障功能:炎症性肠病的潜在治疗靶点

NOD-like receptors mediate homeostatic intestinal epithelial barrier function: promising therapeutic targets for inflammatory bowel disease.

作者信息

Zhou Feng, Zhang Guo Dong, Tan Yang, Hu Shi An, Tang Qun, Pei Gang

机构信息

School of Pharmacy, Hunan University of Chinese Medicine, Changsha, China.

Key Laboratory of Modern Research of TCM, Education Department of Hunan Province, Changsha, China.

出版信息

Therap Adv Gastroenterol. 2023 Sep 9;16:17562848231176889. doi: 10.1177/17562848231176889. eCollection 2023.

Abstract

Inflammatory bowel disease (IBD) is a chronic gastrointestinal inflammatory disease that involves host genetics, the microbiome, and inflammatory responses. The current consensus is that the disruption of the intestinal mucosal barrier is the core pathogenesis of IBD, including intestinal microbial factors, abnormal immune responses, and impaired intestinal mucosal barrier. Cumulative data show that nucleotide-binding and oligomerization domain (NOD)-like receptors (NLRs) are dominant mediators in maintaining the homeostasis of the intestinal mucosal barrier, which play critical roles in sensing the commensal microbiota, maintaining homeostasis, and regulating intestinal inflammation. Blocking NLRs inflammasome activation by botanicals may be a promising way to prevent IBD progression. In this review, we systematically introduce the multiple roles of NLRs in regulating intestinal mucosal barrier homeostasis and focus on summarizing the activities and potential mechanisms of natural products against IBD. Aiming to propose new directions on the pathogenesis and precise treatment of IBD.

摘要

炎症性肠病(IBD)是一种慢性胃肠道炎症性疾病,涉及宿主遗传学、微生物群和炎症反应。目前的共识是,肠道黏膜屏障的破坏是IBD的核心发病机制,包括肠道微生物因素、异常免疫反应和肠道黏膜屏障受损。累积数据表明,核苷酸结合寡聚化结构域(NOD)样受体(NLRs)是维持肠道黏膜屏障稳态的主要介质,在感知共生微生物群、维持稳态和调节肠道炎症中起关键作用。通过植物药阻断NLRs炎性小体激活可能是预防IBD进展的一种有前景的方法。在这篇综述中,我们系统地介绍了NLRs在调节肠道黏膜屏障稳态中的多重作用,并着重总结了天然产物抗IBD的活性及潜在机制。旨在为IBD的发病机制和精准治疗提出新方向。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24a7/10493068/0abbe867fc30/10.1177_17562848231176889-fig1.jpg

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