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Ginsenoside Rg3 inhibits pulmonary fibrosis by preventing HIF-1α nuclear localisation
Zhuo Fu1,2, Yong-Sheng Xu2, Chun-Quan Cai3
1Tianjin Medical University, Tianjin, China.
Background:
Excessive fibroblast proliferation during pulmonary fibrosis leads to structural abnormalities in lung tissue and causes hypoxia and cell injury. However, the mechanisms and effective treatment are still limited.
Methods:
In vivo, we used bleomycin to induce pulmonary fibrosis in mice. IHC and Masson staining were used to evaluate the inhibitory effect of ginsenoside Rg3 in pulmonary fibrosis. In vitro, scanning electron microscopy, transwell and wound healing were used to evaluate the cell phenotype of LL 29 cells. In addition, biacore was used to detect the binding between ginsenoside Rg3 and HIF-1α.
Results:
Here, we found that bleomycin induces the activation of the HIF-1α/TGFβ1 signalling pathway and further enhances the migration and proliferation of fibroblasts through the epithelial mesenchymal transition (EMT). In addition, molecular docking and biacore results indicated that ginsenoside Rg3 can bind HIF-1α. Therefore, Ginsenoside Rg3 can slow down the progression of pulmonary fibrosis by inhibiting the nuclear localisation of HIF-1α.
Conclusions:
This finding suggests that early targeted treatment of hypoxia may have potential value in the treatment of pulmonary fibrosis.
Insights
Ginsenoside Rg3 inhibits fibroblast proliferation and slows pulmonary fibrosis by blocking HIF-1α nuclear localization. Early hypoxia treatment may benefit patients with this lung disease.
Area of Science:
- Pulmonary Medicine
- Cell Biology
- Pharmacology
Background:
- Pulmonary fibrosis involves excessive fibroblast proliferation, leading to lung tissue damage, hypoxia, and cell injury.
- Current understanding of mechanisms and effective treatments for pulmonary fibrosis remains limited.
Purpose of the Study:
- To investigate the mechanism of pulmonary fibrosis induced by bleomycin.
- To evaluate the therapeutic potential of ginsenoside Rg3 in pulmonary fibrosis.
- To determine the interaction between ginsenoside Rg3 and HIF-1α.
Main Methods:
- Pulmonary fibrosis was induced in mice using bleomycin.
- Immunohistochemistry and Masson staining assessed ginsenoside Rg3's inhibitory effects.
- In vitro studies utilized scanning electron microscopy, Transwell, and wound healing assays.
- Biacore analysis and molecular docking were employed to study ginsenoside Rg3 and HIF-1α binding.
Main Results:
- Bleomycin activated the HIF-1α/TGFβ1 pathway, promoting fibroblast migration and proliferation via epithelial-mesenchymal transition (EMT).
- Ginsenoside Rg3 demonstrated binding affinity to HIF-1α through molecular docking and Biacore assays.
- Ginsenoside Rg3 inhibited nuclear localization of HIF-1α, thereby slowing pulmonary fibrosis progression.
Conclusions:
- Ginsenoside Rg3 effectively slows pulmonary fibrosis progression by inhibiting HIF-1α nuclear localization.
- Targeting hypoxia early in pulmonary fibrosis presents a potential therapeutic strategy.
