1. Academic Validation
  2. Refined Murine Model of Idiopathic Pulmonary Fibrosis

Refined Murine Model of Idiopathic Pulmonary Fibrosis

  • J Vis Exp. 2025 Jun 17:(220). doi: 10.3791/68484.
Fengqing Zhu # 1 Jingyu Wang # 2 Wenqing Yang 2 Yonghui He 2 Zhike Liang 3 Shuquan Wei 3 Chuwen Lin 4
Affiliations

Affiliations

  • 1 Department of histology and embryology, School of Medicine, Shenzhen Campus of Sun Yat-Sen University, Sun Yat-Sen University; Department of Pulmonary and Critical Care Medicine, Guangzhou First People's Hospital, School of Medicine, South China University of Technology.
  • 2 Department of histology and embryology, School of Medicine, Shenzhen Campus of Sun Yat-Sen University, Sun Yat-Sen University.
  • 3 Department of Pulmonary and Critical Care Medicine, Guangzhou First People's Hospital, School of Medicine, South China University of Technology.
  • 4 Department of histology and embryology, School of Medicine, Shenzhen Campus of Sun Yat-Sen University, Sun Yat-Sen University; linchw8@mail.sysu.edu.cn.
  • # Contributed equally.
PMID: 40622990 DOI: 10.3791/68484
Abstract

Animal models play a crucial role in understanding disease mechanisms and testing potential therapeutic approaches. However, traditional murine models of idiopathic pulmonary fibrosis (IPF) that rely on a single-dose bleomycin injection fail to accurately replicate the complex pathological features observed in IPF patients. This study introduces an improved method using two successive oropharyngeal administrations of bleomycin in mice, which more effectively mimics the progression of IPF. This novel protocol induces key pathological changes, such as the formation of honeycomb-like cysts, fibroblastic foci, and bronchiolization of the alveolar epithelium, closely resembling the histopathology seen in human IPF. By utilizing this model, we are able to capture the progressive fibrotic changes over a longer time frame, which provides more reliable insights into the pathogenesis of IPF. Furthermore, this two-dose approach offers several advantages over conventional single-dose models, including better reproducibility and a more robust representation of the disease's development. This method enhances our ability to study the mechanisms underlying IPF and evaluate potential therapeutic interventions. The proposed protocol offers significant advancement in preclinical research and provides a valuable tool for investigating both the biology of pulmonary fibrosis and the efficacy of novel treatments.

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