Ginsenoside Rg3 inhibits pulmonary fibrosis by preventing HIF-1α nuclear localisation

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.