Academic Journal
Trilobatin ameliorates dextran sulfate sodium-induced ulcerative colitis in mice via the NF-κB pathway and alterations in gut microbiota
| العنوان: | Trilobatin ameliorates dextran sulfate sodium-induced ulcerative colitis in mice via the NF-κB pathway and alterations in gut microbiota |
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| المؤلفون: | Wang, Nanbo, Li, Zhaohui, Cao, Lingling, Cui, Zhihua |
| المساهمون: | Murayama, Masanori A., Jilin Province Health Talent Special Project, Technology Capacity Enhancement Program of Health Commission of Jilin Province, National College Students Innovation and Entrepreneurship Training Program |
| المصدر: | PLOS ONE ; volume 19, issue 6, page e0305926 ; ISSN 1932-6203 |
| بيانات النشر: | Public Library of Science (PLoS) |
| سنة النشر: | 2024 |
| المجموعة: | PLOS Publications (via CrossRef) |
| الوصف: | Objective This study aimed to evaluate the effects of trilobatin (TLB) on dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) in mice and further explore the underlying mechanisms from the perspectives of signaling pathway and gut microbiota. Methods A mouse model of UC was established using DSS. Trilobatin was administered via oral gavage. Disease severity was assessed based on body weight, disease activity index (DAI), colon length, histological detection, inflammation markers, and colonic mucosal barrier damage. Alternations in the NF-κB and PI3K/Akt pathways were detected by marker proteins. High-throughput 16S rRNA sequencing was performed to investigate the gut microbiota of mice. Results In the DSS-induced UC mice, TLB (30 μg/g) treatment significantly increased the body weight, reduced the DAI score, alleviated colon length shortening, improved histopathological changes in colon tissue, inhibited the secretion and expression of inflammation factors (TNF-α, IL-1β, and IL-6), and increased the expression of tight-junction proteins (ZO-1 and occludin). Furthermore, TLB (30 μg/g) treatment significantly suppressed the activation of NF-κB pathway and altered the composition and diversity of the gut microbiota, as observed in the variations of the relative abundances of Proteobacteria, Actinobacteriota, and Bacteroidota, in UC mice. Conclusion TLB effectively alleviates DSS-induced UC in mice. Regulation of the NF-κB pathway and gut microbiota contributes to TLB-mediated therapeutic effects. Our study not only identified a novel drug candidate for the treatment of UC, but also enhanced our understanding of the biological functions of TLB. |
| نوع الوثيقة: | article in journal/newspaper |
| اللغة: | English |
| DOI: | 10.1371/journal.pone.0305926 |
| الاتاحة: | http://dx.doi.org/10.1371/journal.pone.0305926 https://dx.plos.org/10.1371/journal.pone.0305926 |
| Rights: | http://creativecommons.org/licenses/by/4.0/ |
| رقم الانضمام: | edsbas.27D66980 |
| قاعدة البيانات: | BASE |
| DOI: | 10.1371/journal.pone.0305926 |
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