REVIEW article
Front. Pharmacol.
Sec. Inflammation Pharmacology
Volume 16 - 2025 | doi: 10.3389/fphar.2025.1658772
The Regulatory Effects of Luteolin, Calycosin, and Formononetin on the NLRP3/IL-33/ILC2s Axis in the Treatment of Allergic Rhinitis: Mechanistic Analysis and Therapeutic Potential
Provisionally accepted
- First Affiliated Hospital Guangzhou University of Chinese Medicine, Guangzhou, China
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[Abstract] Allergic rhinitis (AR), a common IgE-mediated inflammatory condition of the nasal mucosa, presents with nasal itching, episodic sneezing, and runny nose. Emerging evidence indicates that type 2 innate lymphoid cells (ILC2s) are key players in AR development. Epithelial-derived alarmins (IL-33, IL-25, TSLP) activate ILC2s, leading to Th2 cytokine production (IL-4, IL-5, IL-13) that enhances inflammation. Recent research shows that NOD-like receptor protein 3 (NLRP3) can function as a transcriptional regulator of interleukin-33 (IL-33), offering new mechanistic insights into ILC2s dysregulation. Based on analysis and pharmacological validation of various effective components against AR, three compounds—luteolin, calycosin, and formononetin—have been identified as key ingredients due to their notable anti-inflammatory properties. This review systematically explores how these compounds regulate the NLRP3/IL-33/ILC2s signaling pathway, laying the groundwork for developing targeted AR treatments.
Keywords: allergic rhinitis, Luteolin, Calycosin, Formononetin, NLRP3/IL-33/ILC2s signaling axis
Received: 03 Jul 2025; Accepted: 17 Sep 2025.
Copyright: © 2025 Jia, Lei, Jiang and Li. 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: Detang Li, lidetang2002@163.com
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