Glucagon like peptide-1 attenuates bleomycin-induced pulmonary fibrosis, involving the inactivation of NF-κB in mice
Abstract
Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease with high mortality and poor prognosis. Previous studies confirmed that NF-κB plays a critical role in the pathogenesis of pulmonary fibrosis and glucagon like peptide-1 (GLP-1) has a property of anti-inflammation by inactivation of NF-κB. Furthermore, the GLP-1 receptor was detected in the lung tissues. Our aim was to investigate the potential value and mechanisms of GLP-1 on BLM-induced pulmonary fibrosis in mice. Mice with BLM-induced pulmonary fibrosis were treated with or without GLP-1 administration. 28 days after BLM infusion, the number of total cells, macrophages, neutrophils, lymphocytes, and the content of TGF-β1 in BALF were measured. Hematoxylin-eosin (HE) staining and Masson's trichrome (MT) staining were performed. The Ashcroft score and hydroxyproline content were analyzed. RT-qPCR and western blot were used to evaluate the expression of α-SMA and VCAM-1. The phosphorylation of NF-κB p65 was also assessed by western blot. DNA binding of NF-κB p65 was measured through Trans(AM) p65 transcription factor ELISA kit. GLP-1 reduced inflammatory cell infiltration and the content of TGF-β1 in BLAF in mice with BLM injection. The Ashcroft score and hydroxyproline content were decreased by GLP-1 administration. Meanwhile, BLM-induced overexpression of α-SMA and VCAM-1 were blocked by GLP-1 treatment in mice. GLP-1 also reduced the ratio of phosphor-NF-κB p65/total-NF-κB p65 and NF-κB p65 DNA binding activity in BLM-induced pulmonary fibrosis in mice. Our data found that BLM-induced lung inflammation and pulmonary fibrosis were significantly alleviated by GLP-1 treatment in mice, possibly through inactivation of NF-κB.
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GLP-1 therapy may be beneficial for the treatment of chronic inflammatory diseases including nonalcoholic steatohepatitis, atherosclerosis, neurodegenerative disorders, diabetic nephropathy, asthma, and psoriasis.
“Thus, GLP-1 therapy may be beneficial for the treatment of chronic inflammatory diseases including nonalcoholic steatohepatitis, atherosclerosis, neurodegenerative disorders, diabetic nephropathy, asthma, and psoriasis [14, 26–32].”
From Anti-Inflammatory Effects of GLP-1-Based Therapies beyond Glucose Control (2016) · cites this paper as [30]
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The Role of GLP-1 Analogues in the Treatment of Obesity-Related Asthma Phenotype
Radzik-Zając, J. (2025) · Biomedicines · doi:10.3390/biomedicines13112610 · Cited by 1 · see citing works
Bobok, N., & Halushko, O. A. (2025) · Problems of ageing and longevity (Ukraine) · doi:10.71012/pro-ageing-2025-4-05 · Cited by 1 · see citing works
Regulation of Immune Responses during Airway Inflammation
Bloodworth, M. H. (2017) · ProQuest Demo Repository
Yang, X., Zhao, G., Bo, Y., Yang, D., Dong, Z., Wu, G., Xu, N., An, M., & Zhao, L. (2021) · SSRN Electronic Journal · doi:10.2139/ssrn.3990206
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- Authors
- GOU, S., ZHU, T., WANG, W., XIAO, M., WANG, X.-C., & CHEN, Z.-H.
- Affiliations
- Sichuan University (CN)
- Venue
- International Immunopharmacology
- Publisher
- Elsevier BV
- Published
- 2014-10
- Volume
- 22
- Issue
- 2
- Pages
- 498-504
- ISSN
- 1567-5769 (ISSN-L)
- OpenAlex
- W1994449362
- Cited by
- 66
- References
- 42
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 6 · 2023: 6 · 2022: 9 · 2021: 6 · 2020: 7 · 2019: 5 · 2018: 6 · 2017: 8 · 2016: 4 · 2015: 4
- FWCI
- 4.25
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- International Immunopharmacology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Pulmonary Hypertension Research and Treatments
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Chronic Obstructive Pulmonary Disease (COPD) Research
- Keywords
- glucagon-like peptide-1, pulmonary fibrosis, bleomycin-induced lung injury, NF-κB, p65 phosphorylation, lung inflammation, TGF-β1, alpha-smooth muscle actin, VCAM-1, idiopathic pulmonary fibrosis, anti-inflammatory therapy
- MeSH terms
- Actins, Animals, Anti-Inflammatory Agents, Antibiotics, Antineoplastic, Bleomycin, Bronchoalveolar Lavage Fluid, Cell Count, Collagen, DNA, Hydroxyproline, Lung, Male, Mice, Inbred C57BL, Pulmonary Fibrosis, NF-kappa B, Vascular Cell Adhesion Molecule-1, Transcription Factor RelA, Glucagon-Like Peptide 1, Transforming Growth Factor beta1
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