ArticleInternational journal of chronic obstructive pulmonary disease2025
Effective-Component Compatibility of Bufei Yishen Formula III Protects Lung Air-Blood Barrier by Regulating the Oxidative Stress: via the Nuclear Factor-E
Article in International journal of chronic obstructive pulmonary disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Research on the Mechanism of Natural Products Acting on Chronic Obstructive Pulmonary Disease.Food science & nutrition · 2026Review
- Effective-Component Compatibility of Bufei Yishen Formula Alleviates Alveolar Epithelial Barrier Damage in COPD Through Inhibition of p38 MAPK Phosphorylation.International journal of chronic obstructive pulmonary disease · 2026Article
- Bu-Fei Yi-Shen Formula Alleviates Oxidative Stress and Improves Airway Epithelial Barrier Dysfunction in COPD.International journal of chronic obstructive pulmonary disease · 2026Article
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Authors and funding
8 authors.
Funding
Abstract
Purpose: Bufei Yishen formula (BYF) is an effective treatment strategy for chronic obstructive pulmonary disease (COPD). Effective-component compatibility of BYF III (ECC-BYF III), composed of 5 active ingredients (ginsenoside Rh1, paeonol, astragaloside, icariin and nobiletin) from BYF, has similar effects to BYF in intervening COPD. The abnormal structure and hypofunction of lung air-blood barrier induces inefficiency gas exchange and promotes development of COPD. However, the role of ECC-BYF III in the air-blood barrier remains unknown. This study dedicated to exploring the effect and mechanism of ECC-BYF III improve structure and function of lung air-blood barrier in COPD. Methods: A COPD rat model was established to study the treatment of ECC-BYF III against COPD. The protective effect of ECC-BYF III on COPD was evaluated through pulmonary function and lung tissue pathology. The structure damage of the lung air-blood barrier was assessed using electron microscopy and immunofluorescence. Finally, we proved the regulating effect of ECC-BYF III in oxidative via the Nrf2 pathway. Results: The ECC-BYF III could significantly alleviate reduced pulmonary function, decrease damage of lung tissue and regulate oxidative stress in COPD rats. And ECC-BYF III reduced thickness of respiratory membrane, ameliorated damage of pulmonary capillary endothelial cells (PCECs) and alveolar epithelial cells (AECs) in COPD rats. Also, ECC-BYF III protected the function and normal cell morphology of type I alveolar epithelial cell (AT I) and type II alveolar epithelial cell (AT II) in COPD rats. Lastly, ECC-BYF III was indicated to adjust the Nrf2 pathway to improve oxidative stress and protect lung air-blood barrier in COPD rats. Conclusion: ECC-BYF III protects lung air-blood barrier in COPD by regulating oxidative stress via Nrf2 pathway.
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