Ginsenoside Rg1 Alleviates Chronic Obstructive Pulmonary Disease Partially Through Regulating ABCB1-Mediated Mitochondrial Dysfunction.
- 1Department of Respiratory Medicine, The Second Affiliated Hospital of Nanjing University of Chinese Medicine & The Second Hospital of Traditional Chinese Medicine in Jiangsu Province, Nanjing, China.
Abstract
To investigate the protective effects of ginsenoside Rg1 on lung injury in chronic obstructive pulmonary disease (COPD) and to elucidate the underlying mechanism involving ATP-binding cassette subfamily B member 1 (ABCB1)-mediated regulation of mitochondrial function. A COPD rat model was established by cigarette smoke exposure, followed by in vivo administration of different doses of ginsenoside Rg1. ABCB1 knockdown was achieved by tail vein injection of short hairpin RNA (shRNA). Hematoxylin and eosin (HE) and Masson staining were performed to evaluate lung histopathology and collagen deposition. Pulmonary function was assessed by measuring inspiratory resistance (Ri), dynamic lung compliance (Cdyn), and the ratio of forced expiratory volume at 0.3 s to forced vital capacity (FEV₀.₃/FVC). In vitro, cigarette smoke extract (CSE) was used to induce injury in human bronchial epithelial (HBE) cells, followed by Rg1 treatment and ABCB1 overexpression or knockdown. Advanced glycation end products-receptor for advanced glycation end products (AGEs-RAGE) and early growth response protein 1-c-Jun N-terminal kinase (EGR1-JNK) signaling pathways were detected. In COPD rats, Rg1 markedly attenuated alveolar structural destruction and collagen deposition, decreased Ri, increased Cdyn and FEV₀.₃/FVC. ABCB1 knockdown partially reversed these protective effects. In HBE cells, Rg1 enhanced cell viability, restored mitochondrial membrane potential, reduced apoptosis, decreased ROS accumulation, and rescued intracellular ATP depletion. Rg1 inhibited the activation of the AGEs-RAGE and EGR1-JNK pathways in a manner associated with upregulation of ABCB1 expression. Ginsenoside Rg1 enhances mitochondrial function partially through upregulation of ABCB1 expression, thereby alleviating mitochondrial dysfunction in COPD rats and CSE-treated HBE cells.
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BibTeX
@article{xu2026ginsenoside,
title = {{Ginsenoside Rg1 Alleviates Chronic Obstructive Pulmonary Disease Partially Through Regulating ABCB1-Mediated Mitochondrial Dysfunction.}},
author = {Wenhui Xu and Jinghong Ye and Kezhou Dong and Zhendong Cao and Yimin Zhu and Lei Li and Baoju Huang},
journal = {Journal of biochemical and molecular toxicology},
year = {2026},
month = oct,
doi = {10.1002/jbt.71160},
url = {https://europepmc.org/article/MED/42952251},
note = {CC BY-NC-ND},
}
RIS
TY - JOUR
TI - Ginsenoside Rg1 Alleviates Chronic Obstructive Pulmonary Disease Partially Through Regulating ABCB1-Mediated Mitochondrial Dysfunction.
AU - Wenhui Xu
AU - Jinghong Ye
AU - Kezhou Dong
AU - Zhendong Cao
AU - Yimin Zhu
AU - Lei Li
AU - Baoju Huang
PY - 2026
DA - 2026/10/28
JO - Journal of biochemical and molecular toxicology
DO - 10.1002/jbt.71160
UR - https://europepmc.org/article/MED/42952251
AB - To investigate the protective effects of ginsenoside Rg1 on lung injury in chronic obstructive pulmonary disease (COPD) and to elucidate the underlying mechanism involving ATP-binding cassette subfamily B member 1 (ABCB1)-mediated regulation of mitochondrial function. A COPD rat model was established by cigarette smoke exposure, followed by in vivo administration of different doses of ginsenoside Rg1. ABCB1 knockdown was achieved by tail vein injection of short hairpin RNA (shRNA). Hematoxylin and eosin (HE) and Masson staining were performed to evaluate lung histopathology and collagen deposition. Pulmonary function was assessed by measuring inspiratory resistance (Ri), dynamic lung compliance (Cdyn), and the ratio of forced expiratory volume at 0.3 s to forced vital capacity (FEV₀.₃/FVC). In vitro, cigarette smoke extract (CSE) was used to induce injury in human bronchial epithelial (HBE) cells, followed by Rg1 treatment and ABCB1 overexpression or knockdown. Advanced glycation end products-receptor for advanced glycation end products (AGEs-RAGE) and early growth response protein 1-c-Jun N-terminal kinase (EGR1-JNK) signaling pathways were detected. In COPD rats, Rg1 markedly attenuated alveolar structural destruction and collagen deposition, decreased Ri, increased Cdyn and FEV₀.₃/FVC. ABCB1 knockdown partially reversed these protective effects. In HBE cells, Rg1 enhanced cell viability, restored mitochondrial membrane potential, reduced apoptosis, decreased ROS accumulation, and rescued intracellular ATP depletion. Rg1 inhibited the activation of the AGEs-RAGE and EGR1-JNK pathways in a manner associated with upregulation of ABCB1 expression. Ginsenoside Rg1 enhances mitochondrial function partially through upregulation of ABCB1 expression, thereby alleviating mitochondrial dysfunction in COPD rats and CSE-treated HBE cells.
SN - 1095-6670
SN - 1099-0461
ER -