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.

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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