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Ginsenoside Rg3 Mitigates LPS-Induced Injury in Human Bronchial Epithelial Cells by Restoring Autophagic Flux and
Xingyu Tao1,2,3,4, Lingjiao Liu1,2,3, Xiaoke Gu5
1Department of Respiratory and Critical Care Medicine, Jiangxi Medical College, Nanchang University, The First Affiliated Hospital, Jiangxi Institute of Respiratory Disease, Nanchang, Jiangxi, 330006, People's Republic of China.
Journal of Inflammation Research
|March 23, 2026
Summary
Ginsenoside Rg3 protects lung cells from injury by restoring autophagy and reducing inflammation. This natural compound shows potential for treating respiratory diseases like COPD.
Area of Science:
- Cell Biology
- Pharmacology
- Immunology
Background:
- Lipopolysaccharide (LPS) induces inflammation and autophagy dysfunction in human bronchial epithelial (HBE) cells.
- Understanding the molecular mechanisms of LPS-induced lung injury is crucial for developing effective treatments.
Purpose of the Study:
- To investigate how ginsenoside Rg3 (G-Rg3) protects HBE cells from LPS-induced damage.
- To elucidate the role of G-Rg3 in regulating autophagic flux and the Toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-κB) inflammatory pathway.
Main Methods:
- HBE cells were exposed to LPS and treated with G-Rg3.
- Western blotting assessed autophagy proteins (ATG4B, ATG7, PIK3C3, LC3B, p62) and TLR4/NF-κB signaling.
- ELISA measured cytokine levels (TNF-α, IL-1β, IL-2, IL-6, IL-8).
- Cell death and apoptosis were analyzed via PI staining and flow cytometry.
Main Results:
- LPS impaired autophagic flux, indicated by increased p62 and LC3B-II.
- G-Rg3 treatment restored autophagic flux.
- G-Rg3 inhibited LPS-induced TLR4/NF-κB activation and reduced pro-inflammatory cytokine secretion.
- G-Rg3 attenuated HBE cell apoptosis and necrosis.
Conclusions:
- Ginsenoside Rg3 mitigates LPS-induced HBE cell injury by restoring autophagic flux and inhibiting the TLR4/NF-κB inflammatory pathway.
- G-Rg3 demonstrates therapeutic potential for respiratory conditions involving inflammation and autophagy dysregulation, such as COPD and acute lung injury.