Related Experiment Video
Updated: Jan 14, 2026
Refined Murine Model of Idiopathic Pulmonary Fibrosis
Published on: June 17, 2025
Ginsenoside Re Inhibits Pulmonary Fibrosis by Regulating CX3CL1/CX3CR1 Axis
Hong Ling1,2, Zhaoqin Wen1,2,3, Hong Xiao1,2
1Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnomedicine of Ministry of Education, Zunyi Medical University, Zunyi, China.
Abstract:
Pulmonary fibrosis is a chronic and irreversible pulmonary disease. At present, there are few drugs to treat pulmonary fibrosis, and effective targets are unknown. This study was aimed at exploring the mechanism of the anti-fibrosis effect of ginsenoside Re (Re). In vivo experiments determined the inhibitory effect of Re on bleomycin (BLM)-induced pulmonary fibrosis and explored whether it was related to the regulation of chemokine CX3C ligand 1 (CX3CL1)/chemokine CX3C receptor 1 (CX3CR1) axis. In vitro experiments, lentivirus transfection was employed to knock down CX3CL1 to further explore the role of the CX3CL1/CX3CR1 axis in the mode of action of Re in inhibiting pulmonary fibrosis. The pathological examination of mice lung tissues showed that Re attenuated BLM-induced pulmonary fibrosis in C57 BL/6J mice. The inhibitory effect of Re on pulmonary fibrosis was more potent in the wild-type mice than that in the CX3CL1-/- mice. Transwell, Western Blot, and RT-qPCR results showed that Re could inhibit TGF-β1-induced epithelial-mesenchymal transition (EMT). In addition, the results showed that epithelial cells inhibited the anti-pulmonary fibrosis effect of Re after CX3CL1 knockdown. The anti-fibrosis effect of Re is related to the regulation of CX3CL1/CX3CR1, and the decreased CX3CL1 gene expression can inhibit the anti-fibrosis effect of Re.
Insights
Ginsenoside Re (Re) effectively treats pulmonary fibrosis by regulating the chemokine CX3CL1/CX3CR1 axis. This mechanism involves inhibiting epithelial-mesenchymal transition (EMT) and restoring Re's anti-fibrosis effects.
Area of Science:
- Pulmonology
- Pharmacology
- Immunology
Background:
- Pulmonary fibrosis is a progressive, irreversible lung disease with limited treatment options.
- Identifying effective therapeutic targets for pulmonary fibrosis remains a significant challenge.
- Ginsenoside Re (Re) is a potential therapeutic agent, but its anti-fibrosis mechanism requires elucidation.
Purpose of the Study:
- To investigate the anti-fibrosis mechanism of ginsenoside Re (Re) in bleomycin (BLM)-induced pulmonary fibrosis.
- To determine if the therapeutic effect of Re involves the regulation of the chemokine CX3C ligand 1 (CX3CL1)/chemokine CX3C receptor 1 (CX3CR1) axis.
- To explore the role of the CX3CL1/CX3CR1 axis in Re's inhibition of epithelial-mesenchymal transition (EMT).
Main Methods:
- In vivo studies using C57 BL/6J mice with BLM-induced pulmonary fibrosis.
- In vitro experiments utilizing lentivirus transfection to knock down CX3CL1 expression.
- Assessment of pulmonary fibrosis, epithelial-mesenchymal transition (EMT), and gene/protein expression via pathological examination, Transwell assays, Western Blot, and RT-qPCR.
Main Results:
- Ginsenoside Re (Re) significantly attenuated BLM-induced pulmonary fibrosis in mice.
- The anti-fibrosis effect of Re was more pronounced in wild-type mice compared to CX3CL1 knockout (CX3CL1-/-) mice.
- Re inhibited TGF-β1-induced EMT, and CX3CL1 knockdown in epithelial cells diminished Re's anti-fibrosis efficacy.
Conclusions:
- The anti-fibrosis effects of Ginsenoside Re (Re) are mediated through the regulation of the CX3CL1/CX3CR1 axis.
- Decreased CX3CL1 gene expression impairs the anti-fibrosis activity of Re.
- Targeting the CX3CL1/CX3CR1 axis represents a potential therapeutic strategy for pulmonary fibrosis.
