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Updated: Jan 13, 2026
07:11
Establishment and Validation of a Rat Model of Pulmonary Arterial Hypertension Associated with Pulmonary Fibrosis
Published on: May 23, 2025
843
Lathyrol Exerts Anti-Pulmonary Fibrosis Effects by Activating PPARγ to Inhibit the TGF-β/Smad Pathway
Qian Zeng1, Min-Lin Liao1, Yu-Yang Luo1
1Xiangya Nursing School, Central South University, 172 Tongzipo Road, Changsha 410013, China.
International Journal of Molecular Sciences
|January 10, 2026
Summary
Lathyrol, a compound from traditional Chinese medicine, effectively treats pulmonary fibrosis by inhibiting fibroblast to myofibroblast transformation. It works by activating PPARγ and suppressing the TGF-β/Smad pathway, offering a potential new therapy for this progressive lung disease.
Area of Science:
- Pharmacology
- Molecular Biology
- Traditional Chinese Medicine
Background:
- Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive lung disease with limited effective drug therapies.
- Lathyrol, a diterpene from *Leptochloa chinensis*, exhibits diverse pharmacological activities.
Purpose of the Study:
- To investigate the anti-pulmonary fibrosis effects of lathyrol.
- To elucidate the underlying molecular mechanisms of lathyrol's action.
Main Methods:
- Established a bleomycin-induced mouse model of pulmonary fibrosis for in vivo studies.
- Utilized TGF-β1 stimulation to induce myofibroblast conversion in fibroblast cell lines for in vitro studies.
- Performed transcriptomic analysis, PPARγ activation assays, and examined Smad3 ubiquitination and nuclear translocation.
Main Results:
- Lathyrol ameliorated lung fibrosis in mice, an effect blocked by a PPARγ inhibitor.
- In vitro, lathyrol inhibited fibroblast to myofibroblast transdifferentiation, dependent on PPARγ activation.
- Lathyrol suppressed phosphorylated Smad3 nuclear translocation and promoted its ubiquitination via Nedd4 and PPARγ interaction.
Conclusions:
- Lathyrol exerts anti-pulmonary fibrosis effects by inhibiting myofibroblast differentiation.
- The mechanism involves PPARγ activation, leading to suppression of the TGF-β/Smad signaling pathway.
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