Shenqi Buzhong Formula ameliorates mitochondrial dysfunction in a rat model of chronic obstructive pulmonary disease by activating the AMPK/SIRT1/PGC-1α pathway.
10.12122/j.issn.1673-4254.2025.05.09
- Author:
Lu ZHANG
1
;
Huanzhang DING
2
;
Haoran XU
1
;
Ke CHEN
1
;
Bowen XU
1
;
Qinjun YANG
3
;
Di WU
1
;
Jiabing TONG
3
;
Zegeng LI
1
Author Information
1. First Affiliated Hospital of Anhui University of Chinese Medicine, Hefei 230031, China.
2. Affiliated First Hospital of Fuyang Normal University, Fuyang 236037, China.
3. Anhui University of Chinese Medicine, Hefei 230038, China.
- Publication Type:Journal Article
- Keywords:
AMPK/SIRT1/PGC-1α pathway;
Shenqi Buzhong Formula;
chronic obstructive pulmonary disease;
mitochondrial biogenesis;
mitochondrial dysfunction
- MeSH:
Animals;
Pulmonary Disease, Chronic Obstructive/drug therapy*;
Drugs, Chinese Herbal/therapeutic use*;
Sirtuin 1/metabolism*;
Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha;
Rats, Sprague-Dawley;
Male;
Rats;
AMP-Activated Protein Kinases/metabolism*;
Mitochondria/metabolism*;
Disease Models, Animal;
Signal Transduction/drug effects*
- From:
Journal of Southern Medical University
2025;45(5):969-976
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVES:To explore the mechanism of Shenqi Buzhong (SQBZ) Formula for alleviating mitochondrial dysfunction in a rat model of chronic obstructive pulmonary disease (COPD) in light of the AMPK/SIRT1/PGC-1α pathway.
METHODS:Fifty male SD rat models of COPD, established by intratracheal lipopolysaccharide (LPS) instillation, exposure to cigarette smoke, and gavage of Senna leaf infusion, were randomized into 5 groups (n=10) for treatment with saline (model group), SQBZ Formula at low, moderate and high doses (3.08, 6.16 and 12.32 g/kg, respectively), or aminophylline (0.024 g/kg) by gavage for 4 weeks, with another 10 untreated rats as the control group. Pulmonary function of the rats were tested, and pathologies and ultrastructural changes of the lung tissues were examined using HE staining and transmission electron microscopy. The levels of SOD, ATP, MDA, and mitochondrial membrane potential in the lungs were detected using WST-1, colorimetric assay, TBA, and JC-1 methods. Flow cytometry was used to analyze ROS level in the lung tissues, and the protein expression levels of P-AMPKα, AMPKα, SIRTI, and PGC-1α were detected using Western blotting.
RESULTS:The rat models of COPD showed significantly decreased lung function, severe histopathological injuries of the lungs, decreased pulmonary levels of SOD activity, ATP and mitochondrial membrane potential, increased levels of MDA and ROS, and decreased pulmonary expressions of P-AMPKα, SIRTI, and PGC-1α proteins. All these changes were significantly alleviated by treatment with SQBZ Formula and aminophylline, and the efficacy was comparable between high-dose SQBZ Formula group and aminophylline group.
CONCLUSIONS:SQBZ Formula ameliorates mitochondrial dysfunction in COPD rats possibly by activating the AMPK/SIRT1/PGC-1α pathway.
