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Updated: Jun 11, 2026

Oropharyngeal Administration of Bleomycin in the Murine Model of Pulmonary Fibrosis
Published on: May 9, 2025
Danthron prevents pulmonary fibrosis through improving mitochondrial function by upregulating carboxylesterase 3
Boyu Li1, Rongman Xu1, Hongyan Zheng1
1Department of Respiratory and Critical Care Medicine, National Clinical Research Center of Respiratory Disease, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Disease, Key Laboratory of Pulmonary Diseases of Health Ministry, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, China.
Danthron, a natural compound, effectively treats pulmonary fibrosis (PF) by improving fibroblast function and enhancing mitochondrial health. This study highlights carboxylesterase 3 (CES3) as a key mediator and potential therapeutic target for PF.
Area of Science:
- Pulmonary Medicine
- Pharmacology
- Cell Biology
Background:
- Idiopathic pulmonary fibrosis (IPF) involves excessive extracellular matrix (ECM) deposition and fibroblast activation.
- Danthron, derived from rhubarb, possesses known antitumor and antioxidant properties.
Purpose of the Study:
- To investigate the therapeutic potential of danthron in pulmonary fibrosis (PF).
- To elucidate the underlying mechanisms of danthron's anti-fibrotic effects.
- To identify novel therapeutic targets for PF.
Main Methods:
- Utilized a bleomycin (BLM)-induced PF mouse model and human precision-cut lung slices (hPCLSs).
- Assessed danthron's effects on histological manifestations and fibrotic markers.
- Explored danthron's impact on human fibroblast function and the role of carboxylesterase 3 (CES3).
Main Results:
- Danthron significantly reduced lung fibrosis in mice and suppressed fibrotic markers in lung tissues and hPCLSs.
- Danthron inhibited fibroblast-to-myofibroblast transition and promoted dedifferentiation.
- The anti-fibrotic effects were linked to CES3 upregulation, enhanced mitochondrial function, and mitophagy, with CES3 inhibition reversing these benefits.
Conclusions:
- Danthron demonstrates significant therapeutic potential for PF in preclinical models.
- Carboxylesterase 3 (CES3) plays a crucial role in danthron's anti-fibrotic mechanism.
- CES3 is identified as a promising therapeutic target for treating PF.
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