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等离子体激活水增强溃疡性结肠炎小鼠模型的肠道屏障功能并减轻炎症。

Plasmon-activated water enhances gut-barrier function and alleviates inflammation in a mouse model of ulcerative colitis.

作者信息

Chang Chun-Chao, Chang Chih-Ju, Liu Chih-Yi, Yeh Hsing-Jung, Li Yu-Ju, Chen Wen-Chao, Chang Chun-Wei, Pan Jun-Liang, Liu Yu-Chuan, Huang Chi-Jung

机构信息

Department of Internal Medicine, Division of Gastroenterology and Hepatology, Taipei Medical University Hospital, Taipei 110301, Taiwan, R.O.C.

Department of Internal Medicine, Division of Gastroenterology and Hepatology, School of Medicine, College of Medicine, Taipei Medical University, Taipei 110301, Taiwan, R.O.C.

出版信息

Exp Ther Med. 2025 May 27;30(1):146. doi: 10.3892/etm.2025.12896. eCollection 2025 Jul.

DOI:10.3892/etm.2025.12896
PMID:40496763
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12150364/
Abstract

Ulcerative colitis (UC) is a chronic, relapsing inflammatory bowel disease characterized by disruption of the intestinal epithelial barrier and alterations in mucosal gene expression associated with intestinal integrity. Given the risks associated with UC, novel therapies capable of restoring intestinal barrier function and inhibiting inflammation are needed. Plasmon-activated water (PAW) is a nontoxic form of water with potential in the treatment of inflammatory diseases. The aim of the present study was to evaluate the therapeutic effects of PAW in a murine model of UC. Histological and immunohistochemical analyses were performed on colon tissues from mice with dextran sodium sulfate (DSS)-induced UC treated with either 5-aminosalicylic acid (5-ASA) or PAW. Epithelial cell density was decreased in the DSS model mice compared with that in the normal control mice, whereas treatment with 5-ASA or PAW attenuated this DSS-induced reduction. Microscopy revealed that the DSS/PAW group exhibited significantly reduced epithelial loss, crypt damage and inflammatory cell infiltration compared with that in the DSS group. In addition, immunohistochemical analysis demonstrated that PAW downregulated the DSS-induced expression of tumor necrosis factor-α and keratin 20 in epithelial cells and the lamina propria. Furthermore, PAW also attenuated the DSS-induced loss of expression of three proteins essential for cell adhesion and tight junctions, namely E-cadherin (CDH1), tight junction protein 1 (ZO-1) and occludin, in the colonic epithelium, particularly in intestinal crypts. In addition, mucin 1 (MUC1) expression was decreased and MUC2 expression increased in the mucosal layer of the colons of the DSS/PAW group compared with those in the DSS group. In conclusion, the colonic mucosa is a reliable site for evaluating epithelial damage and inflammatory infiltration. PAW ameliorated DSS-induced UC in mice by modulating the expression of key barrier-associated proteins, including CDH1, occludin, ZO-1, MUC1 and MUC2. These findings highlight the therapeutic potential of PAW in the treatment of colitis.

摘要

溃疡性结肠炎（UC）是一种慢性复发性炎症性肠病，其特征是肠道上皮屏障破坏以及与肠道完整性相关的黏膜基因表达改变。鉴于UC相关的风险，需要能够恢复肠道屏障功能并抑制炎症的新疗法。等离子体激活水（PAW）是一种无毒形式的水，在治疗炎症性疾病方面具有潜力。本研究的目的是评估PAW在UC小鼠模型中的治疗效果。对用葡聚糖硫酸钠（DSS）诱导的UC小鼠结肠组织进行组织学和免疫组织化学分析，这些小鼠分别用5-氨基水杨酸（5-ASA）或PAW治疗。与正常对照小鼠相比，DSS模型小鼠的上皮细胞密度降低，而用5-ASA或PAW治疗可减轻DSS诱导的这种降低。显微镜检查显示，与DSS组相比，DSS/PAW组的上皮损失、隐窝损伤和炎性细胞浸润明显减少。此外，免疫组织化学分析表明，PAW下调了DSS诱导的上皮细胞和固有层中肿瘤坏死因子-α和角蛋白20的表达。此外，PAW还减轻了DSS诱导的结肠上皮细胞，特别是肠隐窝中对细胞黏附和紧密连接至关重要的三种蛋白质，即E-钙黏蛋白（CDH1）、紧密连接蛋白1（ZO-1）和闭合蛋白的表达损失。此外，与DSS组相比，DSS/PAW组结肠黏膜层中黏蛋白1（MUC1）表达降低，MUC2表达增加。总之，结肠黏膜是评估上皮损伤和炎性浸润的可靠部位。PAW通过调节关键屏障相关蛋白（包括CDH1、闭合蛋白、ZO-1、MUC1和MUC2）的表达改善了DSS诱导的小鼠UC。这些发现突出了PAW在治疗结肠炎方面的治疗潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e55/12150364/10df35a75b14/etm-30-01-12896-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e55/12150364/e79d61df6ce2/etm-30-01-12896-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e55/12150364/5f021299e674/etm-30-01-12896-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e55/12150364/60ca95e906db/etm-30-01-12896-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e55/12150364/29111419ea97/etm-30-01-12896-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e55/12150364/013606938286/etm-30-01-12896-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e55/12150364/c4c58c040637/etm-30-01-12896-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e55/12150364/10df35a75b14/etm-30-01-12896-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e55/12150364/e79d61df6ce2/etm-30-01-12896-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e55/12150364/5f021299e674/etm-30-01-12896-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e55/12150364/60ca95e906db/etm-30-01-12896-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e55/12150364/29111419ea97/etm-30-01-12896-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e55/12150364/013606938286/etm-30-01-12896-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e55/12150364/c4c58c040637/etm-30-01-12896-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e55/12150364/10df35a75b14/etm-30-01-12896-g06.jpg

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本文引用的文献

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Adaptive Metabolic Responses Facilitate Blood-Brain Barrier Repair in Ischemic Stroke via BHB-Mediated Epigenetic Modification of ZO-1 Expression.

Adv Sci (Weinh). 2024-7

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Resolvins protect against diabetes-induced colonic oxidative stress, barrier dysfunction, and associated diarrhea via the HO-1 pathway.

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Costs of medications used to treat inflammatory bowel disease.

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