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Updated: Aug 17, 2026

A Mouse Model of Pulmonary Fibrosis Induced by Nasal Bleomycin Nebulization
Published on: January 20, 2023
[The role of oxygen radicals in bleomycin-induced pulmonary fibrosis]
1Respiratory Disease Research Laboratory, Union Hospital, Tongji Medical University Wuhan.
Abstract:
A model of pulmonary fibrosis in rat has been developed using intratracheal administration of bleomycin (BLM) A5 (5mg/kg). Histopathologic features and total lung collagen were studied. We found that type I pneumocytes detached, basement membrane denuded and endothelia edema were the earliest changes in BLM induced pulmonary fibrosis. Serum MDA (an index of lipid peroxidation) level in rats receiving intratracheal bleomycin were increased at earlier time after bleomycin administration. Meanwhile, MDA level in the lung homogenate was elevated too. Our results indicated that the injured type I pneumocytes and endothelia caused by oxygen radicles are the fundamental damages in bleomycin-induced pulmonary fibrosis.
Insights
Bleomycin-induced pulmonary fibrosis in rats shows early damage to lung cells and increased lipid peroxidation. Oxygen radicals are identified as the primary cause of these fundamental damages.
Area of Science:
- Pulmonary Medicine
- Toxicology
- Cell Biology
Background:
- Pulmonary fibrosis is a debilitating lung disease.
- Bleomycin (BLM) is a chemotherapeutic agent that can induce pulmonary fibrosis.
- Understanding the early mechanisms of BLM-induced lung injury is crucial for developing treatments.
Purpose of the Study:
- To establish a rat model of pulmonary fibrosis using bleomycin.
- To investigate the early histopathologic changes and biochemical markers in bleomycin-induced pulmonary fibrosis.
- To identify the fundamental cellular damage and causative agents in this fibrotic model.
Main Methods:
- Intratracheal administration of bleomycin (5 mg/kg) in rats.
- Histopathologic examination of lung tissue.
- Measurement of total lung collagen.
- Quantification of serum and lung homogenate malondialdehyde (MDA) levels.
Main Results:
- Early changes included type I pneumocyte detachment, basement membrane denudation, and endothelial edema.
- Serum and lung homogenate MDA levels, an indicator of lipid peroxidation, were elevated following bleomycin administration.
- These findings suggest a significant role for oxidative stress in the pathogenesis.
Conclusions:
- The rat model effectively replicates key features of pulmonary fibrosis.
- Injured type I pneumocytes and endothelial cells, caused by oxygen radicals, are fundamental to bleomycin-induced pulmonary fibrosis.
- Lipid peroxidation is an important biochemical marker of early lung injury in this model.
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