Inhaled exogenous thymosin beta 4 suppresses bleomycin-induced pulmonary fibrosis in mice via TGF-β1 signalling pathway

J Pharm Pharmacol. 2025 Apr 3;77(4):582-592. doi: 10.1093/jpp/rgae143.

Abstract

Objectives: Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, and fibrotic interstitial lung disease. The two drugs indicated for IPF have limited efficacy and there is an urgent need to develop new drugs. Thymosin β4 (Tβ4) is a natural endogenous repair factor whose antifibrotic effects have been reported. This study aimed to evaluate the effect of exogenous recombinant human thymosin beta 4 (rhTβ4) on pulmonary fibrosis.

Methods: Pulmonary fibrosis was induced in mice with bleomycin, and rhTβ4 was administrated by nebulization following three strategies: early dosing, mid-term dosing, and late dosing. The rhTβ4 efficacy was assessed by hydroxyproline, lung function, and lung histopathology. In vitro, the effects of rhTβ4 on fibroblast and lung epithelial cell phenotypes, as well as the TGF-β1 pathway, were evaluated.

Key findings: Aerosol administration of rhTβ4 could alleviate bleomycin-induced pulmonary fibrosis in mice at different stages of fibrosis. Studies conducted in vitro suggested that rhTβ4 could suppress lung fibroblasts from proliferating, migrating, and activation via regulating the TGF-β1 signalling pathway. In vitro, rhTβ4 also inhibited the epithelial-mesenchymal transition-like process of pulmonary epithelial cells.

Conclusions: This study suggests that nebulized rhTβ4 is a potential treatment for IPF.

Keywords: TGF-β1; idiopathic pulmonary fibrosis; inhalation; myofibroblasts; thymosin β4.

MeSH terms

  • Administration, Inhalation
  • Animals
  • Bleomycin
  • Cell Proliferation / drug effects
  • Disease Models, Animal
  • Epithelial Cells / drug effects
  • Epithelial Cells / metabolism
  • Epithelial-Mesenchymal Transition / drug effects
  • Fibroblasts / drug effects
  • Fibroblasts / metabolism
  • Humans
  • Idiopathic Pulmonary Fibrosis* / chemically induced
  • Idiopathic Pulmonary Fibrosis* / drug therapy
  • Idiopathic Pulmonary Fibrosis* / metabolism
  • Lung / drug effects
  • Lung / metabolism
  • Lung / pathology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Pulmonary Fibrosis* / chemically induced
  • Pulmonary Fibrosis* / drug therapy
  • Pulmonary Fibrosis* / metabolism
  • Recombinant Proteins / administration & dosage
  • Recombinant Proteins / pharmacology
  • Signal Transduction / drug effects
  • Thymosin* / administration & dosage
  • Thymosin* / pharmacology
  • Transforming Growth Factor beta1* / metabolism

Substances

  • Bleomycin
  • Thymosin
  • thymosin beta(4)
  • Transforming Growth Factor beta1
  • Recombinant Proteins