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Updated: Jan 26, 2026

Oropharyngeal Administration of Bleomycin in the Murine Model of Pulmonary Fibrosis
Published on: May 9, 2025
Inhibitory effects of total ginsenoside on bleomycin-induced pulmonary fibrosis in mice
Lu Yang1, Pan-Pan Chen1, Min Luo2
1Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnomedicine of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou, 563006, China.
Abstract:
Pulmonary fibrosis is the final outcome of a variety of diffuse pulmonary interstitial diseases, and it has an unclear pathogenesis. There is no effective drug treatment, so the clinical prognosis is poor. As an effective component of ginseng, total ginsenoside (TG) inhibits acute lung injury. This study determined whether TG has protective effects on pulmonary fibrosis and investigated its protective mechanisms. A pulmonary fibrosis model in BALB/c mice was established by injecting the bleomycin chemotherapeutic agent into the trachea. TG (40, 80, and 160 mg/kg/d) was given continuously for 28 days from the second day after development of the model. Pulmonary fibrosis was determined by measuring the lung coefficient, haematoxylin and eosin, and Masson's trichrome staining of lung samples, and detection of alpha smooth muscle actin expression in lung tissues. To investigate the mechanisms of anti-pulmonary fibrosis by TG, we detected the genes and proteins of the transforming growth factor-β1 (TGF-β1)/Smad signalling pathway and matrix metalloproteinase (MMP) system. Treatment with TG (40, 80, and 160 mg/kg/d) ameliorated pulmonary fibrosis induced by bleomycin in mice, downregulated the expression of TGF-β1, Smad2, Smad3, MMP-2, MMP-9, and tissue inhibitor of metalloproteinase-1, and upregulated the protein expression of Smad7. These results suggest that the protective effects of TG on pulmonary fibrosis induced by bleomycin are related to regulation of the TGF-β1/Smad signalling pathway and MMP system.
Insights
Total ginsenoside (TG), a ginseng component, shows promise in treating pulmonary fibrosis. TG ameliorates bleomycin-induced lung injury in mice by regulating key signaling pathways and matrix metalloproteinases.
Area of Science:
- Pulmonology
- Pharmacology
- Cell Biology
Background:
- Pulmonary fibrosis, a severe outcome of interstitial lung diseases, lacks effective treatments and has poor prognosis.
- Total ginsenoside (TG), derived from ginseng, is known to inhibit acute lung injury.
Purpose of the Study:
- To evaluate the protective effects of TG against pulmonary fibrosis.
- To elucidate the underlying mechanisms of TG's action in pulmonary fibrosis.
Main Methods:
- A bleomycin-induced pulmonary fibrosis model was established in BALB/c mice.
- Mice were treated with varying doses of TG (40, 80, 160 mg/kg/d) for 28 days.
- Pulmonary fibrosis was assessed via lung coefficient, histological staining (H&E, Masson's trichrome), and alpha-smooth muscle actin expression.
- The transforming growth factor-β1 (TGF-β1)/Smad signaling pathway and matrix metalloproteinase (MMP) system were analyzed at the gene and protein levels.
Main Results:
- TG treatment significantly ameliorated bleomycin-induced pulmonary fibrosis in mice.
- TG downregulated the expression of TGF-β1, Smad2, Smad3, MMP-2, MMP-9, and tissue inhibitor of metalloproteinase-1.
- TG upregulated the protein expression of Smad7.
Conclusions:
- Total ginsenoside (TG) exhibits protective effects against bleomycin-induced pulmonary fibrosis.
- TG's mechanism involves the regulation of the TGF-β1/Smad signaling pathway and the MMP system.
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