Bu-Fei Formula Ameliorates Inflammation in a Preclinical COPD-Like Model by Targeting Mitochondrial Hyperactivity to Inhibit the NLRP3 Inflammasome

Background: Chronic Obstructive Pulmonary Disease (COPD) is characterized by persistent airflow limitation and chronic airway inflammation. While the traditional Chinese medicine Bu-Fei Formula (BFF) effectively ameliorates COPD symptoms clinically, however, the precise molecular mechanisms underlying its therapeutic effects remain a knowledge gap. Methods: The therapeutic effects and anti-inflammatory mechanisms of BFF in COPD were investigated using cigarette smoke + LPS-induced COPD-like rats and CSE-stimulated macrophages. BFF treatment was administered in both models for 8 weeks in a dose-dependent manner. Lung injury, collagen deposition, and macrophage ultrastructure were assessed by H&E, Masson’s staining, and TEM. The evaluation of IL-1β, IL-18, NLRP3, ASC, and Caspase-1 p20 expression was performed via ELISA, IHC, IF, and Western blot. Oxidative stress (MDA, SOD) and mitochondrial function (complexes I–V, ATP, ROS) were also evaluated. Results: BFF treatment produced a pronounced improvement in lung pathology of COPD-like rats, characterized by alleviation of tissue damage, suppression of inflammatory and alveolar degeneration, and reduction of collagen accumulation in the interstitium. It also ameliorated inflammatory injury at the cellular level by inhibiting macrophage pyroptosis. Mechanistically, BFF suppressed the overexpression of mitochondrial respiratory chain complexes I–V. It reduced the levels of ROS, ATP, MDA, NLRP3, ASC, Caspase-1 p20, IL-1β, and IL-18, while enhancing SOD activity. These findings suggest that BFF mitigates the inflammatory damage in COPD by suppressing the hyperactivation of mitochondrial energy metabolism, enhancing the efficiency of the oxidative respiratory chain, and reducing ROS production, and suppressing the NLRP3 inflammasome response. Keywords: Bu-Fei formula, inflammation, NLRP3 Inflammasome, mitochondrial respiratory chain complexes, chronic obstructive pulmonary disease

Authors

Institutions

Publication Details

Journal
International Journal of COPD
Published
2026-05-01
DOI
https://doi.org/10.2147/copd.s586009
Primary Topic
Chronic Obstructive Pulmonary Disease (COPD) Research
Type
article
Field-Weighted Citation Impact
0.00
Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

Bu-Fei Formula Ameliorates Inflammation in a Preclinical COPD-Like Model by Targeting Mitochondrial Hyperactivity to Inhibit the NLRP3 Inflammasome

Lu Liu, Yanjie Liu, Jiangqin Ou, Genyan Liu et al.
International Journal of COPD
Chronic Obstructive Pulmonary Disease (COPD) Research
article

Bu-Fei Formula Ameliorates Inflammation in a Preclinical COPD-Like Model by Targeting Mitochondrial Hyperactivity to Inhibit the NLRP3 Inflammasome

Lu Liu, Yanjie Liu, Jiangqin Ou, Genyan Liu, Jiayin Ning, Xingli Sun, Tong Yang
article en

Abstract

Background: Chronic Obstructive Pulmonary Disease (COPD) is characterized by persistent airflow limitation and chronic airway inflammation. While the traditional Chinese medicine Bu-Fei Formula (BFF) effectively ameliorates COPD symptoms clinically, however, the precise molecular mechanisms underlying its therapeutic effects remain a knowledge gap. Methods: The therapeutic effects and anti-inflammatory mechanisms of BFF in COPD were investigated using cigarette smoke + LPS-induced COPD-like rats and CSE-stimulated macrophages. BFF treatment was administered in both models for 8 weeks in a dose-dependent manner. Lung injury, collagen deposition, and macrophage ultrastructure were assessed by H&E, Masson’s staining, and TEM. The evaluation of IL-1β, IL-18, NLRP3, ASC, and Caspase-1 p20 expression was performed via ELISA, IHC, IF, and Western blot. Oxidative stress (MDA, SOD) and mitochondrial function (complexes I–V, ATP, ROS) were also evaluated. Results: BFF treatment produced a pronounced improvement in lung pathology of COPD-like rats, characterized by alleviation of tissue damage, suppression of inflammatory and alveolar degeneration, and reduction of collagen accumulation in the interstitium. It also ameliorated inflammatory injury at the cellular level by inhibiting macrophage pyroptosis. Mechanistically, BFF suppressed the overexpression of mitochondrial respiratory chain complexes I–V. It reduced the levels of ROS, ATP, MDA, NLRP3, ASC, Caspase-1 p20, IL-1β, and IL-18, while enhancing SOD activity. These findings suggest that BFF mitigates the inflammatory damage in COPD by suppressing the hyperactivation of mitochondrial energy metabolism, enhancing the efficiency of the oxidative respiratory chain, and reducing ROS production, and suppressing the NLRP3 inflammasome response. Keywords: Bu-Fei formula, inflammation, NLRP3 Inflammasome, mitochondrial respiratory chain complexes, chronic obstructive pulmonary disease

International Journal of COPDVol. Volume 21
Guiyang College of Traditional Chinese Medicine (CN), Guiyang Medical University (CN), Affiliated Hospital of Guizhou Medical University (CN), Guizhou Provincial People's Hospital (CN)
Affordable and clean energy, Good health and well-being
Openalex Percentile: Top 5%
Chronic Obstructive Pulmonary Disease (COPD) Research
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.