ORIGINAL RESEARCH article
Front. Immunol.
Sec. Mucosal Immunity
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1587479
This article is part of the Research TopicNatural Products and Intestinal Mucosal ImmunityView all 9 articles
Kurarinone ameliorates intestinal mucosal inflammation via regulating T cell immunity
Provisionally accepted- Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, Chengdu, China
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Inflammatory bowel disease (IBD) has become an increasingly significant global health concern, imposing substantial economic and psychological burdens on society and public health systems. Herbal medicines, which have shown promise in alleviating IBD symptoms and promoting remission through mechanisms such as immune regulation and anti-inflammatory effects, are gaining increasing attention. Kurarinone (KAR) is a major component of the dried roots of Sophora flavescens, which exhibits a range of pharmacological activities, including antioxidant and anti-inflammatory effects.However, research on the therapeutic potential of KAR in IBD, particularly its effect on intestinal mucosal inflammation, remains limited. Here, we demonstrated that administration of KAR resulted in a mitigated colonic tissue damage in mice with trinitrobenzene sulfonic acid (TNBS)-induced colitis and decreased the infiltration of inflammatory cells, including monocytes/macrophages, neutrophils, and T lymphocytes. Moreover, KAR protected TNBS-insulted mice from colonic goblet cell loss and tight junction destruction. Furthermore, KAR treatment led to the restoration of the gut microbiota to a more normal composition. Mechanistically, KAR suppressed T helper (Th) 17 cell response but facilitated interleukin (IL)-10 production via Blimp-1. Our study investigated the impact of KAR on mice with TNBS-induced colitis and elucidated its underlying mechanisms, thereby uncovering novel possibilities for clinical interventions in IBD.
Keywords: Kurarinone, experimental colitis, inflammatory bowel disease, Intestinal epithelial barrier, Th17 Cells
Received: 04 Mar 2025; Accepted: 11 Apr 2025.
Copyright: © 2025 Pan, Deng, Wang, Zhou, Wang, Gao and He. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Chong He, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, Chengdu, China
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