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.

Abstract

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, 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: , 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., 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.