Phytomedicine : international journal of phytotherapy and phytopharmacology · 2026
Palmatine restores airway epithelial barrier function of asthma by inhibiting Alox15-mediated ferroptosis.
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Zhao Lei, Wu Jifei, Zhang Yichen, Zhao Yongchang, Lin Yanmei, Zhang Min, Bao Wuping
Аннотация
BACKGROUND: Epithelial barrier dysfunction plays a key role in asthma pathogenesis. Palmatine has been shown to reinforce epithelial integrity in colitis and ameliorate urticaria-like skin inflammation, suggesting potential barrier-protective effects.
PURPOSE: To investigate the barrier-protective role of palmatine in eosinophilic asthma.
STUDY DESIGN AND METHODS: An ovalbumin-induced eosinophilic asthma model was established. After palmatine administration, lung function, airway responsiveness, mucus secretion, collagen deposition, and epithelial barrier integrity were assessed. Proteomics, molecular docking, cellular experiments, and immunofluorescence were performed to elucidate underlying mechanisms.
RESULTS: Palmatine markedly restored epithelial barrier integrity by upregulating E-cadherin, occludin, and ZO-1. Correspondingly, it improved both large- and small-airway obstruction, and reduced airway hyperresponsiveness. It also reduced IL-5, IL-13, and MMP9 levels, indicating attenuation of inflammation and collagen deposition. Proteomics and mechanistic studies revealed that palmatine suppressed Alox15-mediated ferroptosis in airway epithelial cells, reflected by reduced GSSG, MDA, and LPO and increased GSH levels in lung tissue. In erastin-treated BEAS-2B cells, palmatine inhibited Alox15 and PEBP1 expression accompanied by recovery of epithelial junction proteins E-cadherin, occludin, and ZO-1.
CONCLUSION: Palmatine exhibits therapeutic effects in eosinophilic asthma. By inhibiting Alox15-mediated ferroptosis, it restores airway epithelial barrier integrity and alleviates inflammation and airway hyperresponsiveness, highlighting its promise as a potential therapeutic agent for eosinophilic asthma.
PURPOSE: To investigate the barrier-protective role of palmatine in eosinophilic asthma.
STUDY DESIGN AND METHODS: An ovalbumin-induced eosinophilic asthma model was established. After palmatine administration, lung function, airway responsiveness, mucus secretion, collagen deposition, and epithelial barrier integrity were assessed. Proteomics, molecular docking, cellular experiments, and immunofluorescence were performed to elucidate underlying mechanisms.
RESULTS: Palmatine markedly restored epithelial barrier integrity by upregulating E-cadherin, occludin, and ZO-1. Correspondingly, it improved both large- and small-airway obstruction, and reduced airway hyperresponsiveness. It also reduced IL-5, IL-13, and MMP9 levels, indicating attenuation of inflammation and collagen deposition. Proteomics and mechanistic studies revealed that palmatine suppressed Alox15-mediated ferroptosis in airway epithelial cells, reflected by reduced GSSG, MDA, and LPO and increased GSH levels in lung tissue. In erastin-treated BEAS-2B cells, palmatine inhibited Alox15 and PEBP1 expression accompanied by recovery of epithelial junction proteins E-cadherin, occludin, and ZO-1.
CONCLUSION: Palmatine exhibits therapeutic effects in eosinophilic asthma. By inhibiting Alox15-mediated ferroptosis, it restores airway epithelial barrier integrity and alleviates inflammation and airway hyperresponsiveness, highlighting its promise as a potential therapeutic agent for eosinophilic asthma.