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清肠栓修复溃疡性结肠炎肠黏膜屏障的机制

Mechanism of Qingchang Suppository on repairing the intestinal mucosal barrier in ulcerative colitis.

作者信息

Shan Jingyi, Liu Suxian, Liu Haoyue, Yuan Jianye, Lin Jiang

机构信息

Department of Gastroenterology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China.

Institute of Digestive Diseases, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China.

出版信息

Front Pharmacol. 2023 Aug 22;14:1221849. doi: 10.3389/fphar.2023.1221849. eCollection 2023.

DOI:10.3389/fphar.2023.1221849
PMID:37675045
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10478270/
Abstract

Ulcerative colitis (UC) is a refractory inflammatory bowel disease, and the outcomes of conventional therapies of UC, including 5-aminosalicylic acid, glucocorticoids, immunosuppressants, and biological agents, are not satisfied with patients and physicians with regard to adverse reactions and financial burden. The abnormality of the intestinal mucosal barrier in the pathogenesis of UC was verified. Qingchang Suppository (QCS) is an herbal preparation and is effective in treating ulcerative proctitis. The mechanism of QCS and its active ingredients have not been concluded especially in mucosal healing. This review elucidated the potential mechanism of QCS from the intestinal mucosal barrier perspective to help exploring future QCS research directions.

摘要

溃疡性结肠炎(UC)是一种难治性炎症性肠病,包括5-氨基水杨酸、糖皮质激素、免疫抑制剂和生物制剂在内的UC传统治疗方法,在不良反应和经济负担方面,患者和医生都不满意。UC发病机制中肠黏膜屏障的异常已得到证实。清肠栓(QCS)是一种草药制剂,对治疗溃疡性直肠炎有效。QCS及其活性成分的作用机制尚未明确,尤其是在黏膜愈合方面。本综述从肠黏膜屏障角度阐明了QCS的潜在作用机制,以帮助探索未来QCS的研究方向。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a84c/10478270/47f5f0d41a7a/fphar-14-1221849-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a84c/10478270/47f5f0d41a7a/fphar-14-1221849-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a84c/10478270/47f5f0d41a7a/fphar-14-1221849-g001.jpg

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Polysaccharides Modulate Intestinal Microflora in Aged Rats .多糖对老年大鼠肠道微生物群的调节作用
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Portulaca oleracea L. Extract Ameliorates Intestinal Inflammation by Regulating Endoplasmic Reticulum Stress and Autophagy.
马齿苋提取物通过调节内质网应激和自噬缓解肠道炎症。
Mol Nutr Food Res. 2022 Mar;66(5):e2100791. doi: 10.1002/mnfr.202100791. Epub 2022 Jan 9.
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MUC2 and related bacterial factors: Therapeutic targets for ulcerative colitis.黏蛋白 2 及其相关细菌因素:溃疡性结肠炎的治疗靶点。
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Exploring the Mechanism of Indigo Naturalis in the Treatment of Ulcerative Colitis Based on TLR4/MyD88/NF-κB Signaling Pathway and Gut Microbiota.基于TLR4/MyD88/NF-κB信号通路和肠道微生物群探讨青黛治疗溃疡性结肠炎的机制
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Gallic acid mitigates LPS-induced inflammatory response via suppressing NF-κB signalling pathway in IPEC-J2 cells.没食子酸通过抑制 IPEC-J2 细胞 NF-κB 信号通路减轻 LPS 诱导的炎症反应。
J Anim Physiol Anim Nutr (Berl). 2022 Sep;106(5):1000-1008. doi: 10.1111/jpn.13612. Epub 2021 Jul 20.
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