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. 2024 Dec 9;15:1485255. doi: 10.3389/fphar.2024.1485255

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Copyright © 2024 Jiang, Yan, Qin, Liu, Duan, Wang, Zhang, Lin, Li, Xie and Ke.

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) and the copyright owner(s) 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.

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Workflow for analyzing Que’s mechanisms in UC treatment. Network pharmacology, in conjunction with transcriptomic methodologies and experimental validation, demonstrated that quercetin alleviated the symptoms associated with DSS-induced colitis. It attenuates the inflammatory response, promotes the repair of colonic mucosal tissues, and elevates the levels of colonic tight junction proteins in mice with ulcerative colitis. These effects may enhance tight junction integrity and restore intestinal barrier function by modulating the IL-17A signaling pathway while simultaneously inhibiting the CXCL8-CXCR1/2 axis.