ORIGINAL RESEARCH article
Front. Immunol.
Sec. Inflammation
This article is part of the Research TopicWhat's on the Horizon for Asthma Treatment?View all 5 articles
Anti-Inflammatory Effects of 1,8-cineol via NF-κB/COX-2 pathway in BEAS-2B cells and alleviates bronchoconstriction and airway hyperreactivity in ovalbumin sensitized mice
Provisionally accepted
- 1The Second Affiliated Hospital Zhejiang University School of Medicine, Hangzhou, China
- 2Zhejiang Chinese Medical University, Hangzhou, China
- 3Zhujiang Hospital of Southern Medical University, Guangzhou, China
- 4Hangzhou First People's Hospital, Hangzhou, China
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Objective: Asthma is a chronic inflammatory airway disease characterized by airway remodeling and hyperresponsiveness, driven in part by TGF-β1-induced epithelial-mesenchymal transition (EMT). The natural compound 1,8-cineol, derived from Eucalyptus globulus, has shown anti-inflammatory potential. This study aimed to investigate its protective effects against EMT and airway inflammation via the NF-κB/COX-2 pathway. Methods: In vivo, ovalbumin-sensitized BALB/c mice were treated with 1,8-cineol (50 mg/kg) to evaluate airway resistance, lung compliance, and inflammatory markers (IgE, IL-4, IL-13, IL-17). Histopathological changes were assessed via H&E and PAS staining. In vitro, TGF-β1-stimulated BEAS-2B cells were treated with 1,8-cineol to analyze EMT markers (α-SMA, E-cadherin, N-cadherin), migration capacity, and NF-κB/COX-2 signaling using RT-qPCR, Western blotting, and transwell assays. Results: 1,8-cineol significantly attenuated airway hyperresponsiveness and reduced EMT markers (α-SMA, N-cadherin) in OVA-sensitized mice, while improving lung compliance. In BEAS-2B cells, it suppressed TGF-β1-induced EMT and migration without cytotoxicity. Mechanistically, 1,8-cineol downregulated NF-κB phosphorylation and COX-2 expression. OVA challenge elevated serum IgE and BALF cytokines (IL-4, IL-13, IL-17), which were mitigated by 1,8-cineol. Conclusions: 1,8-cineol inhibits TGF-β1-driven EMT and airway inflammation by modulating the NF-κB/COX-2 pathway, highlighting its therapeutic potential for asthma.
Keywords: 1,8-cineol, airway inflammation, Airway Remodeling, NF-κB/COX-2 pathway, Ovalbumin-induced acute asthma, Th2 cytokine
Received: 28 Sep 2025; Accepted: 12 Jan 2026.
Copyright: © 2026 Wang, Zhu, Zhang, Tong and Xu. 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:
Fei Tong
Qiaoping Xu
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