Introduction
Pulmonary fibrosis (PF) is a chronic, progressive lung disease that leads to impaired gas exchange function, respiratory failure, and even death. The onset and progression of the disease are initiated by early pulmonary inflammation induced by various factors; the persistence of this inflammation results in the deposition of fibrous tissue within the lungs, thereby triggering pulmonary fibrosis. Studies have shown that aberrant activation and differentiation of pulmonary fibroblasts are among the pathogenic factors, while persistent alveolar injury and incomplete repair can also promote pulmonary fibrosis.
Disease models
The SMOC has long been dedicated to autoimmune disease research and has developed a variety of pulmonary fibrosis models, all of which exhibit good phenotypes, providing powerful tools for the efficacy evaluation and safety assessment of related drugs.
Bleomycin (BLM) is an anti‑cancer drug that has toxic side effects on the lungs. It induces DNA strand breaks and oxidative stress, thereby causing parenchymal inflammation, epithelial cell injury accompanied by reactive hyperplasia, epithelial‑mesenchymal transition, fibroblast activation and differentiation into myofibroblasts, as well as damage to the basement membrane and alveolar epithelium.
Fig.1 Bleomycin induced pulmonary fibrosis in C57BL/6 (male, 10-12w) mice. (A) Body Weight. (B) Body Weight Change. (C) Survival Curve.
Fig2.Bleomycin induced pulmonary fibrosis in C57BL/6 (male, 10-12w) mice. (A) H&E and Masson stain. (B) Alveolar inflammation score. (C)Alveolar fibrosis score.
