Allergy, asthma & immunology research · 2026
Eucalyptol-Limonene-Pinene Attenuates Mucus Hypersecretion and Inflammation via Multitarget Mechanisms in Chronic Rhinosinusitis With Nasal Polyps.
СтатьяНазвание и аннотация: Перевод в очереди
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Zhang Yuan, Jiao Jian, Zhuang Mengyan, Zhang Qinqin, He Ting, Li Ying, Sima Yutong, Wang Xiangdong, Zhang Luo
Аннотация
PURPOSE: Chronic rhinosinusitis with nasal polyps (CRSwNP) is a common chronic inflammatory disease of the mucosa, which significantly impairs patients' quality of life. Eucalyptol-Limonene-Pinene (ELP) is a plant-derived mucoactive agent used in respiratory diseases, including CRSwNP; however, its underlying mechanisms remain unclear. This study aimed to evaluate ELP's effect on CRSwNP and explore its mechanisms.
METHODS: Predicted targets and pathways from network pharmacology were validated in vitro using nasal epithelial cells (NECs) and single-cell suspensions from CRSwNP patients, and in vivo using Aspergillus oryzae protease/ovalbumin-induced mouse CRSwNP model. Quantitative real-time polymerase chain reaction, enzyme-linked immunosorbent assay, Western blot, Luminex, hematoxylin and eosin staining, Alcian blue-periodic acid-Schiff staining, immunofluorescence, and immunohistochemistry were used to quantify inflammatory mediators and mucociliary changes.
RESULTS: Network pharmacology revealed that epidermal growth factor receptor (EGFR), hypoxia-inducible factor 1-alpha, interleukin (IL)-2 are core targets and enriched in inflammation pathways. In vitro, ELP inhibited the overexpression of mucin 5AC induced by amphiregulin, hypoxia, IL-2 and IL-13 in NECs. ELP decreased expression of type 2 inflammatory mediators, arachidonate 15-lipoxygenase, C-C motif chemokine ligand 26, periostin and epithelial-derived alarmins thymic stromal lymphopoietin, IL-33 in NECs, reduced the concentrations of cytokines/chemokines and countered lipopolysaccharide-induced inflammation in single-cell suspensions. In vivo, ELP reduced epithelial thickness, inflammatory infiltration, goblet cell hyperplasia and cilia damage.
CONCLUSIONS: ELP reduced mucus hypersecretion and inflammatory mediators in vitro and in vivo in CRSwNP by specifically inhibiting EGFR-, hypoxia-, IL-2- and IL-13-mediated pathways, suppressing inflammatory responses, and alleviating ciliary damage, suggesting its potential therapeutic value.
METHODS: Predicted targets and pathways from network pharmacology were validated in vitro using nasal epithelial cells (NECs) and single-cell suspensions from CRSwNP patients, and in vivo using Aspergillus oryzae protease/ovalbumin-induced mouse CRSwNP model. Quantitative real-time polymerase chain reaction, enzyme-linked immunosorbent assay, Western blot, Luminex, hematoxylin and eosin staining, Alcian blue-periodic acid-Schiff staining, immunofluorescence, and immunohistochemistry were used to quantify inflammatory mediators and mucociliary changes.
RESULTS: Network pharmacology revealed that epidermal growth factor receptor (EGFR), hypoxia-inducible factor 1-alpha, interleukin (IL)-2 are core targets and enriched in inflammation pathways. In vitro, ELP inhibited the overexpression of mucin 5AC induced by amphiregulin, hypoxia, IL-2 and IL-13 in NECs. ELP decreased expression of type 2 inflammatory mediators, arachidonate 15-lipoxygenase, C-C motif chemokine ligand 26, periostin and epithelial-derived alarmins thymic stromal lymphopoietin, IL-33 in NECs, reduced the concentrations of cytokines/chemokines and countered lipopolysaccharide-induced inflammation in single-cell suspensions. In vivo, ELP reduced epithelial thickness, inflammatory infiltration, goblet cell hyperplasia and cilia damage.
CONCLUSIONS: ELP reduced mucus hypersecretion and inflammatory mediators in vitro and in vivo in CRSwNP by specifically inhibiting EGFR-, hypoxia-, IL-2- and IL-13-mediated pathways, suppressing inflammatory responses, and alleviating ciliary damage, suggesting its potential therapeutic value.