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Updated: May 11, 2026
A Mouse Model of Pulmonary Fibrosis Induced by Nasal Bleomycin Nebulization
Published on: January 20, 2023
Huangqi Guizhi Wuwu Decoction attenuates bleomycin-induced pulmonary fibrosis via modulating TGF-β/Smad and
Yuanmei Bai1, Peilin Li1, Cailing Gan1
1Department of Respiratory and Critical Care Medicine, Center for High Altitude Medicine, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, China.
Background:
Pulmonary fibrosis (PF) is a progressive interstitial lung disease with limited pharmacotherapy and frequent adverse effects, prompting safer multi-target options from traditional medicines.
Purpose:
To determine whether Huangqi Guizhi Wuwu Decoction (HGD) mitigates PF and to elucidate mechanisms.
Study Design:
Integrated in vivo bleomycin (BLM) induced mouse PF models (preventive and therapeutic regimens) with in vitro TGF-β1 driven assays in human pulmonary fibroblasts (HPFs), NIH/3T3 cells and A549 epithelial cells; nintedanib served as a positive control.
Methods:
Evaluated lung histopathology (H&E, Masson), collagen accumulation, fibroblast activation and epithelial mesenchymal transition (EMT) markers; quantified TGF-β/Smad signaling (p-Smad2/3) and profiled pulmonary immune subsets (macrophages, DCs, MDSCs). Performed RNA-seq on TGF-β1-stimulated NIH/3T3 cells and network pharmacology analyses to prioritize pathways and targets, followed by immunoblotting and functional validation.
Results:
HGD attenuated BLM-induced lung injury and collagen deposition, suppressed fibroblast activation, reversed epithelial EMT, and reduced pulmonary accumulation of macrophages, DCs and MDSCs. HGD decreased p-Smad2/3 in lung tissues and fibroblasts. Transcriptomics plus target-network analysis highlighted cell-cycle pathways, with experimental data supporting their modulation consistent with anti-fibrotic activity. No overt toxicity was observed at the tested doses.
Conclusion:
HGD exerts multi-target anti-fibrotic effects in BLM-induced PF, associated with inhibition of canonical TGF-β/Smad signaling, rebalancing of the pulmonary immune microenvironment and modulation of cell-cycle, supporting further development of HGD as an adjunct strategy for PF.
Insights
Huangqi Guizhi Wuwu Decoction (HGD) shows promise in treating pulmonary fibrosis (PF) by reducing lung injury and inflammation. This traditional medicine offers a safer, multi-target approach to combatting this progressive lung disease.
Area of Science:
- Traditional Chinese Medicine
- Pulmonary Fibrosis Research
- Pharmacology
Background:
- Pulmonary fibrosis (PF) is a progressive lung disease with limited treatment options and significant side effects.
- There is a need for safer, multi-target therapeutic strategies for PF, particularly from traditional medicine.
Purpose of the Study:
- To investigate the efficacy of Huangqi Guizhi Wuwu Decoction (HGD) in mitigating pulmonary fibrosis.
- To elucidate the underlying mechanisms of HGD's anti-fibrotic effects.
Main Methods:
- Utilized bleomycin (BLM)-induced mouse models of pulmonary fibrosis (PF) and in vitro assays with human pulmonary fibroblasts and epithelial cells.
- Assessed lung histopathology, collagen deposition, fibroblast activation, epithelial-mesenchymal transition (EMT), TGF-β/Smad signaling, and pulmonary immune cell populations.
- Employed RNA-sequencing and network pharmacology to identify key pathways and targets, followed by experimental validation.
Main Results:
- HGD significantly attenuated BLM-induced lung injury, collagen deposition, and fibroblast activation.
- HGD reversed epithelial-mesenchymal transition (EMT) and reduced pro-fibrotic immune cell accumulation in the lungs.
- HGD inhibited TGF-β/Smad signaling and modulated cell-cycle pathways, demonstrating anti-fibrotic activity without observed toxicity.
Conclusions:
- Huangqi Guizhi Wuwu Decoction (HGD) exhibits multi-target anti-fibrotic effects in a preclinical model of pulmonary fibrosis.
- HGD's mechanisms involve inhibiting TGF-β/Smad signaling, rebalancing the pulmonary immune microenvironment, and modulating cell-cycle pathways.
- HGD represents a potential adjunct therapy for pulmonary fibrosis, warranting further clinical development.
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