Phytomedicine : international journal of phytotherapy and phytopharmacology · 2026
Ecklonia cava extract attenuates PM-exacerbated allergic asthma by modulating pulmonary macrophage polarization to suppress macrophage extracellular trap (MET) formation.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Kim Hyo Jin, Thilakarathna Manathunge Kumudu Sulakshani, Yang Jiwon, Dayaddra Gamaralalage Prabhavi, Ko Mi-Ok, Herath Kalahe Hewage Iresha Nadeeka Madushani, Kang Minhyeok, Jeon You-Jin, Ko Seung Mi, Choi Soo Youn, Kim Chan Young, Jee Youngheun
Аннотация
BACKGROUND: Environmental particulate matter (PM) exacerbates allergic airway inflammation and promotes oxidative stress-driven immune dysregulation. Pulmonary macrophages are key mediators of these responses, and their polarization contributes to Th2/Th17-associated asthma pathology. Ecklonia cava ethanol extract (ECE), an edible brown alga, has anti-inflammatory potential.
PURPOSE: This study investigated whether ECE attenuates PM-exacerbated allergic airway inflammation by regulating oxidative stress, pulmonary macrophage polarization, and macrophage extracellular trap (MET) formation.
STUDY DESIGN: MLE-12 lung epithelial cells and a PM-exacerbated allergic asthma mouse model were used to evaluate the protective effects of ECE.
METHODS: PM-induced oxidative stress and NF-κB activation were assessed in MLE-12 cells. In vivo, airway hyperresponsiveness, inflammatory cell infiltration, epithelial injury, mast cell activation, Th2/Th17 cytokine responses, oxidative stress in pulmonary macrophage, macrophage polarization, and MET formation were analyzed. A PAD4 inhibition model was used to evaluate CitH3-associated macrophage responses.
RESULTS: ECE suppressed PM-induced ROS production, MDA accumulation, p-IκBα expression, and NF-κB reporter activity in MLE-12 cells, with NAC supporting the involvement of oxidative stress. In PM-exacerbated allergic asthma mice, ECE reduced airway hyperresponsiveness, BALF inflammatory cells and protein levels, histopathological injury, mast cell degranulation, serum histamine, and Th2/Th17-associated cytokines. ECE also attenuated oxidative stress in pulmonary macrophage, reduced M1-associated markers, including CD80, Nos2, and iNOS, and suppressed M2-associated markers, including CD206, Arg1, and p-STAT6. Moreover, ECE decreased MET-related markers, including MPO, histone H3, MPO/CitH3, and F4/80/CitH3-positive macrophages. PAD4 inhibition further supported the involvement of CitH3-associated MET responses.
CONCLUSION: ECE mitigates PM-exacerbated allergic airway inflammation by suppressing epithelial oxidative stress and NF-κB activation, in association with attenuated pulmonary macrophage polarization and MET formation. These findings suggest that ECE protects against PM-aggravated allergic asthma through coordinated regulation of oxidative stress and macrophage-mediated inflammatory responses.
PURPOSE: This study investigated whether ECE attenuates PM-exacerbated allergic airway inflammation by regulating oxidative stress, pulmonary macrophage polarization, and macrophage extracellular trap (MET) formation.
STUDY DESIGN: MLE-12 lung epithelial cells and a PM-exacerbated allergic asthma mouse model were used to evaluate the protective effects of ECE.
METHODS: PM-induced oxidative stress and NF-κB activation were assessed in MLE-12 cells. In vivo, airway hyperresponsiveness, inflammatory cell infiltration, epithelial injury, mast cell activation, Th2/Th17 cytokine responses, oxidative stress in pulmonary macrophage, macrophage polarization, and MET formation were analyzed. A PAD4 inhibition model was used to evaluate CitH3-associated macrophage responses.
RESULTS: ECE suppressed PM-induced ROS production, MDA accumulation, p-IκBα expression, and NF-κB reporter activity in MLE-12 cells, with NAC supporting the involvement of oxidative stress. In PM-exacerbated allergic asthma mice, ECE reduced airway hyperresponsiveness, BALF inflammatory cells and protein levels, histopathological injury, mast cell degranulation, serum histamine, and Th2/Th17-associated cytokines. ECE also attenuated oxidative stress in pulmonary macrophage, reduced M1-associated markers, including CD80, Nos2, and iNOS, and suppressed M2-associated markers, including CD206, Arg1, and p-STAT6. Moreover, ECE decreased MET-related markers, including MPO, histone H3, MPO/CitH3, and F4/80/CitH3-positive macrophages. PAD4 inhibition further supported the involvement of CitH3-associated MET responses.
CONCLUSION: ECE mitigates PM-exacerbated allergic airway inflammation by suppressing epithelial oxidative stress and NF-κB activation, in association with attenuated pulmonary macrophage polarization and MET formation. These findings suggest that ECE protects against PM-aggravated allergic asthma through coordinated regulation of oxidative stress and macrophage-mediated inflammatory responses.