Ginsenoside Rg3 Mitigates LPS-Induced Injury in Human Bronchial Epithelial Cells by Restoring Autophagic Flux and Inhibiting the TLR4/NF-κB-Mediated Inflammatory Response

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Xingyu Tao,1– 4,* Lingjiao Liu,1– 3,* Xiaoke Gu,5 Baohui Jia,6 Qi Yu,1– 3 Yingying Wei,1– 3 Wei Zhang,1– 3 Jing Zhou1– 3 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; 2Jiangxi Clinical Research Center for Respiratory Diseases, Nanchang, Jiangxi, 330006, People’s Republic of China; 3China-Japan Friendship Jiangxi Hospital, National Regional Center for Respiratory Medicine, Nanchang, Jiangxi, 330200, People’s Republic of China; 4Department of Respiratory and Critical Care Medicine, The Third Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, People’s Republic of China; 5Department of Anesthesia, Sun Yat-Sen University Sixth Affiliated Hospital, Guangzhou, Guangdong, 510000, People’s Republic of China; 6Department of Respiratory and Critical Care Medicine, The Fourth Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, 330006, People’s Republic of China*These authors contributed equally to this workCorrespondence: Jing Zhou, Department 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, Email ndyfy02118@ncu.edu.cn Xingyu Tao, Department 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, Email cshi42345@gmail.com; 353006220005@email.ncu.edu.cnPurpose: To elucidate the molecular mechanism by which ginsenoside Rg3 (G-Rg3) protects human bronchial epithelial (HBE) cells against lipopolysaccharide (LPS)-induced injury, focusing on its regulation of autophagic flux and the TLR4/NF-κB-mediated inflammatory pathway.Methods: HBE cells were treated with LPS (1– 100 ng/mL) to induce autophagy dysregulation and inflammation. G-Rg3 (2– 16 μM) was administered to evaluate its protective effects. Western blotting was used to detect autophagy-related proteins (ATG4B, ATG7, PIK3C3, LC3B, p62) and TLR4/NF-κB signaling molecules; ELISA quantified proinflammatory cytokines (TNF-α, IL-1β, IL-2, IL-6, IL-8); PI staining and flow cytometry analyzed cell death and apoptosis.Results: LPS dose-dependently upregulated the expression of autophagy-related proteins (ATG4B, ATG7, PIK3C3, p62, LC3B-II), with accumulated p62 and LC3B-II indicating impaired clearance of autophagic substrates. Additionally, G-Rg3 inhibited LPS-induced TLR4/NF-κB activation, suppressed proinflammatory cytokine secretion, and attenuated HBE cell apoptosis/necrosis.Conclusion: G-Rg3 mitigates LPS-induced HBE cell injury by dual mechanisms: restoring impaired autophagic flux and inhibiting the TLR4/NF-κB inflammatory cascade. These findings identify G-Rg3 as a promising therapeutic agent targeting the crosstalk between autophagy and inflammation in respiratory diseases such as COPD and acute lung injury.Keywords: Ginsenoside Rg3, autophagy, LPS, HBE, cell death

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