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已发表论文
人参皂苷Rg3通过恢复自噬通量并抑制TLR4/NF-κB介导的炎症反应减轻LPS诱导的人支气管上皮细胞损伤
Authors Tao X, Liu L, Gu X, Jia B, Yu Q, Wei Y, Zhang W, Zhou J
Received 20 July 2025
Accepted for publication 25 December 2025
Published 20 January 2026 Volume 2026:19 555053
DOI https://doi.org/10.2147/JIR.S555053
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Tara Strutt
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 work
Correspondence: 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.cn
Purpose: 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
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 work
Correspondence: 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.cn
Purpose: 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