ArticleMolecular biology reports2024
The role of quercetin in ameliorating bleomycin-induced pulmonary fibrosis: insights into autophagy and the SIRT1/AMPK signaling pathway.
Article in Molecular biology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- AI-driven discovery of natural product-derived FAK1 inhibitors for idiopathic pulmonary fibrosis.Molecular diversity · 2026Article
- Molecular insights into the anti-inflammatory and antifibrotic effects of licorice-ginger decoction in experimental models of inflammatory arthritis-associated lung fibrosis.Immunology and cell biology · 2026Article
- Protective effect of cannabinoid type II receptor ligand on bleomycin-induced pulmonary fibrosis in mice.PloS one · 2026Article
- AMPK/SIRT1/PGC-1α Signaling Pathway: Molecular Mechanisms and Targeted Strategies From Energy Homeostasis Regulation to Disease Therapy.CNS neuroscience & therapeutics · 2025Review
- Review
- Mechanism study of the effects of astragaloside IV and quercetin on idiopathic pulmonary fibrosis.Journal of natural medicines · 2025Article
- Review
- FBR2 modulates ferroptosis via the SIRT3/p53 pathway to ameliorate pulmonary fibrosis.Frontiers in pharmacology · 2025Article
- Melittin alleviates bleomycin-induced pulmonary fibrosisIranian journal of basic medical sciences · 2025Article
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Authors and funding
8 authors.
Funding
Abstract
backgroundIdiopathic pulmonary fibrosis (IPF) is a disease of unknown etiology characterized by a constant incidence rate. Unfortunately, effective pharmacological treatments for this condition are lacking and the identification of novel therapeutic approaches and underlying pathological mechanisms are required. This study investigated the potential of quercetin in alleviating pulmonary fibrosis by promoting autophagy and activation of the SIRT1/AMPK pathway.
methodsMouse models of IPF were divided into four treatment groups: control, bleomycin (BLM), quercetin (Q), and quercetin + EX-527 (Q + E) treatment. Pulmonary fibrosis was induced in the mouse models through intratracheal instillation of BLM. Various indexes were identified through histological staining, Western blotting analysis, enzyme-linked immunosorbent assay, immunohistochemistry, and transmission electron microscopy.
resultsQuercetin treatment ameliorated the pathology of BLM-induced pulmonary fibrosis of mice by reducing α-smooth muscle actin (α-SMA), collagen I (Col I), and collagen III (Col III) levels, and also improved the level of E-cadherin in lung tissue. Furthermore, Quercetin significantly enhanced LC3II/LC3I levels, decreased P62 expression, and increased the number of autophagosomes in lung tissue. These effects were accompanied by the activation of the SIRT1/AMPK pathway. Treatment with EX-527, an inhibitor for SIRT1, reversed all effects induced by quercetin.
conclusionThis study showed that quercetin could alleviate pulmonary fibrosis and improve epithelial-mesenchymal transition by acting on the SIRT1/AMPK signaling pathway, which may be achieved by regulating the level of autophagy.
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