Abstract

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.

Details

Title
Ginsenoside Rg3 inhibits pulmonary fibrosis by preventing HIF-1α nuclear localisation
Author
Fu, Zhuo; Yong-sheng, Xu; Chun-quan, Cai  VIAFID ORCID Logo 
Pages
1-10
Section
Research article
Publication year
2021
Publication date
2021
Publisher
BioMed Central
e-ISSN
14712466
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
2502998628
Copyright
© 2021. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.