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Updated: Oct 26, 2025
07:51
Refined Murine Model of Idiopathic Pulmonary Fibrosis
Published on: June 17, 2025
465
Pterostilbene alleviates pulmonary fibrosis by regulating ASIC2
Yanfang Peng1, Yingwen Zhang2, Yabing Zhang1
1Department of Traditional Chinese Medicine, Zhongnan Hospital of Wuhan University, No. 169 Donghu Road, Wuchang District, Wuhan, 430071, Hubei, China.
Chinese Medicine
|July 29, 2021
Summary
Pterostilbene (PTE) shows antifibrotic activity against idiopathic pulmonary fibrosis (IPF) by inhibiting EMT and ECM accumulation. This study suggests PTE may be a potential IPF treatment by downregulating ASIC2.
Area of Science:
- Pulmonary Medicine
- Cell Biology
- Pharmacology
Background:
- Idiopathic pulmonary fibrosis (IPF) is a chronic respiratory disease with limited treatment options and adverse effects.
- Current treatments for IPF have shortcomings and associated adverse effects.
- Evaluating novel antifibrotic agents is crucial for IPF management.
Purpose of the Study:
- To investigate the antifibrotic effects of pterostilbene (PTE) in an in vitro model of IPF.
- To determine the mechanism by which PTE exerts its antifibrotic activity.
- To assess PTE's impact on key fibrotic pathways including epithelial-mesenchymal transition (EMT), extracellular matrix (ECM) accumulation, autophagy, and apoptosis.
Main Methods:
- An in vitro IPF model was established using A549 and alveolar epithelial cells (AECs) treated with transforming growth factor-β1 (TGF-β1).
- Cells were treated with pterostilbene (PTE) at 30 μmol/L to evaluate its effects on EMT, ECM, autophagy, and apoptosis.
- Western blot, flow cytometry, and transcriptome high-throughput sequencing were employed to analyze cellular changes and gene expression, including the role of acid sensing ion channel subunit 2 (ASIC2).
Main Results:
- TGF-β1 induced EMT, ECM accumulation, and inhibited autophagy and apoptosis in lung cells.
- PTE treatment significantly inhibited TGF-β1-induced pulmonary fibrosis, reducing EMT and ECM accumulation while restoring autophagy and apoptosis.
- Transcriptome analysis revealed that PTE downregulates ASIC2, and ASIC2 overexpression reversed the protective effects of PTE, indicating PTE acts by downregulating ASIC2.
Conclusions:
- Pterostilbene (PTE) demonstrates significant antifibrotic activity in an in vitro model of idiopathic pulmonary fibrosis.
- PTE inhibits pulmonary fibrosis by downregulating acid sensing ion channel subunit 2 (ASIC2).
- PTE and ASIC2 inhibitors represent potential therapeutic strategies for future IPF treatment.
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