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传统医学缓解溃疡性结肠炎的机制:调节肠道屏障功能。

The mechanism of traditional medicine in alleviating ulcerative colitis: regulating intestinal barrier function.

作者信息

Xu Qiuyun, Yao Yuan, Liu Yongchao, Zhang Jie, Mao Liming

机构信息

Department of Immunology, School of Medicine, Nantong University, Nantong, Jiangsu, China.

Basic Medical Research Center, School of Medicine, Nantong University, Nantong, China.

出版信息

Front Pharmacol. 2023 Oct 9;14:1228969. doi: 10.3389/fphar.2023.1228969. eCollection 2023.

DOI:10.3389/fphar.2023.1228969
PMID:37876728
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10590899/
Abstract

Ulcerative colitis (UC) is an idiopathic inflammatory disease mainly affects the large bowel and the rectum. The pathogenesis of this disease has not been fully elucidated, while the disruption of the intestinal barrier function triggered by various stimulating factors related to the host genetics, immunity, gut microbiota, and environment has been considered to be major mechanisms that affect the development of UC. Given the limited effective therapies, the treatment of this disease is not ideal and its incidence and prevalence are increasing. Therefore, developing new therapies with high efficiency and efficacy is important for treating UC. Many recent studies disclosed that numerous herbal decoctions and natural compounds derived from traditional herbal medicine showed promising therapeutic activities in animal models of colitis and have gained increasing attention from scientists in the study of UC. Some of these decoctions and compounds can effectively alleviate colonic inflammation and relieve clinical symptoms in animal models of colitis via regulating intestinal barrier function. While no study is available to review the underlying mechanisms of these potential therapies in regulating the integrity and function of the intestinal barrier. This review aims to summarize the effects of various herbal decoctions or bioactive compounds on the severity of colonic inflammation via various mechanisms, mainly including regulating the production of tight junction proteins, mucins, the composition of gut microbiota and microbial-associated metabolites, the infiltration of inflammatory cells and mediators, and the oxidative stress in the gut. On this basis, we discussed the related regulators and the affected signaling pathways of the mentioned traditional medicine in modulating the disruption or restoration of the intestinal barrier, such as NF-κB/MAPK, PI3K, and HIF-1α signaling pathways. In addition, the possible limitations of current studies and a prospect for future investigation and development of new UC therapies are provided based on our knowledge and current understanding. This review may improve our understanding of the current progression in studies of traditional medicine-derived therapies in protecting the intestinal barrier function and their roles in alleviating animal models of UC. It may be beneficial to the work of researchers in both basic and translational studies of UC.

摘要

溃疡性结肠炎(UC)是一种特发性炎症性疾病,主要影响大肠和直肠。该病的发病机制尚未完全阐明,而由宿主遗传学、免疫、肠道微生物群和环境等多种刺激因素引发的肠道屏障功能破坏被认为是影响UC发生发展的主要机制。鉴于有效治疗方法有限,该病的治疗并不理想,且其发病率和患病率正在上升。因此,开发高效有效的新疗法对治疗UC至关重要。最近的许多研究表明,许多传统草药煎剂和天然化合物在结肠炎动物模型中显示出有前景的治疗活性,并在UC研究中受到科学家越来越多的关注。其中一些煎剂和化合物可通过调节肠道屏障功能有效减轻结肠炎动物模型中的结肠炎症并缓解临床症状。然而,尚无研究综述这些潜在疗法调节肠道屏障完整性和功能的潜在机制。本综述旨在总结各种草药煎剂或生物活性化合物通过多种机制对结肠炎症严重程度的影响,主要包括调节紧密连接蛋白、黏蛋白的产生,肠道微生物群及其相关代谢产物的组成,炎症细胞和介质的浸润,以及肠道中的氧化应激。在此基础上,我们讨论了上述传统药物在调节肠道屏障破坏或修复中的相关调节因子和受影响的信号通路,如NF-κB/MAPK、PI3K和HIF-1α信号通路。此外,基于我们的知识和当前理解,提供了当前研究可能存在的局限性以及UC新疗法未来研究和开发的前景。本综述可能会增进我们对传统药物衍生疗法在保护肠道屏障功能及其在减轻UC动物模型中的作用研究的当前进展的理解。这可能对UC基础研究和转化研究的研究人员的工作有益。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af30/10590899/d455439ccda1/fphar-14-1228969-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af30/10590899/4255eefd05ab/fphar-14-1228969-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af30/10590899/d455439ccda1/fphar-14-1228969-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af30/10590899/4255eefd05ab/fphar-14-1228969-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af30/10590899/d455439ccda1/fphar-14-1228969-g002.jpg

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