Ginsenoside Rg3 Inhibits Pulmonary Fibrosis by Preventing HIF-1α Nuclear Localisation

Abstract Introduction: 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 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 of ginsenoside Rg3 and HIF-1α. Results : Here, we find 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). Ginsenoside Rg3 can slow down the progression of pulmonary fibrosis by inhibiting the nuclear localisation of HIF-1α. In addition, molecular docking and biacore experiments indicated that ginsenoside Rg3 can bind HIF-1α and restrict the progression of pulmonary fibrosis in animals. Hypoxia can lead to excessive proliferation of lung fibroblasts and further accelerate lung fibrosis. Conclusions : This finding suggests that early targeted treatment of hypoxia may have potential value in the treatment of pulmonary fibrosis.