ArticleRespiratory research2022
Nifuroxazide ameliorates pulmonary fibrosis by blocking myofibroblast genesis: a drug repurposing study.
Article in Respiratory research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 35 citations in OpenAlex.
- Pharmacological repurposing of cilostazol to attenuate the progression of pulmonary fibrosis: efficacy validation via integrated network pharmacology and in vivo experimentation.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Geranylgeranylacetone Alleviates Pulmonary Fibrosis in Mice by Activation of Nrf2 /HO-1/NQO1 Pathway.Cell biochemistry and biophysics · 2026Article
- Heart-Lung Interactions in Gas Exchange: From Physiology to Pathophysiology.Comprehensive Physiology · 2026Review
- Leucine Mitigates Diabetic Nephropathy via Its Antioxidant Effect and Modulation of TGF-β/SMAD-3 Signalling Pathway in Streptozotocin-Induced Diabetic Rats.Drug design, development and therapy · 2026Article
- Review
- Investigation of the protective effect of cilostazol on acute lung injury-mediated inflammation and in silico molecular modelling studies of inflammatory signalling pathway: a repurposing study.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Nifuroxazide and 4-Hydroxybenzhydrazone Derivatives as New Antiparasitic (Pharmaceutics · 2025Article
- Pulmonary hypertension: etiology and anti-inflammatory treatment pathways of natural products.Frontiers in pharmacology · 2025Review
- Integrated ML-Based Strategy Identifies Drug Repurposing for Idiopathic Pulmonary Fibrosis.ACS omega · 2024Article
- Niclosamide - encapsulated lipid nanoparticles for the reversal of pulmonary fibrosis.Materials today. Bio · 2024Article
- Dapagliflozin can alleviate renal fibrosis in rats with streptozotocin‑induced type 2 diabetes mellitus.Experimental and therapeutic medicine · 2023Article
- Searching for Novel Candidate Small Molecules for Ameliorating Idiopathic Pulmonary Fibrosis: a Narrative Review.Biomolecules & therapeutics · 2023Review
- Niclosamide-loaded nanoparticles (Ncl-NPs) reverse pulmonary fibrosis in vivo and in vitro.Journal of advanced research · 2023Article
- The Existing Drug Nifuroxazide as an Antischistosomal Agent:Microbiology spectrum · 2023Article
- Nifuroxazide induces the apoptosis of human non‑small cell lung cancer cells through the endoplasmic reticulum stress PERK signaling pathway.Oncology letters · 2023Article
- Early Endothelial Signaling Transduction in Developing Lung Edema.Life (Basel, Switzerland) · 2023Review
- The impact of heterogeneity of the air-blood barrier on control of lung extravascular water and alveolar gas exchange.Frontiers in network physiology · 2023Review
- Research Progress in the Molecular Mechanisms, Therapeutic Targets, and Drug Development of Idiopathic Pulmonary Fibrosis.Frontiers in pharmacology · 2022Review
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
backgroundIdiopathic pulmonary fibrosis (IPF) is a serious interstitial lung disease with a complex pathogenesis and high mortality. The development of new drugs is time-consuming and laborious; therefore, research on the new use of old drugs can save time and clinical costs and even avoid serious side effects. Nifuroxazide (NIF) was originally used to treat diarrhoea, but more recently, it has been found to have additional pharmacological effects, such as anti-tumour effects and inhibition of inflammatory diseases related to diabetic nephropathy. However, there are no reports regarding its role in pulmonary fibrosis.
methodsThe therapeutic effect of NIF on pulmonary fibrosis in vivo was measured by ELISA, hydroxyproline content, H&E and Masson staining, immunohistochemistry (IHC) and western blot. Immune cell content in lung tissue was also analysed by flow cytometry. NIF cytotoxicity was evaluated in NIH/3T3 cells, human pulmonary fibroblasts (HPFs), A549 cells and rat primary lung fibroblasts (RPLFs) using the MTT assay. Finally, an in vitro cell model created by transforming growth factor-β1 (TGF-β1) stimulation was assessed using different experiments (immunofluorescence, western blot and wound migration assay) to evaluate the effects of NIF on the activation of NIH/3T3 and HPF cells and the epithelial-mesenchymal transition (EMT) and migration of A549 cells.
resultsIn vivo, intraperitoneal injection of NIF relieved and reversed pulmonary fibrosis caused by bleomycin (BLM) bronchial instillation. In addition, NIF inhibited the expression of a variety of cellular inflammatory factors and immune cells. Furthermore, NIF suppressed the activation of fibroblasts and EMT of epithelial cells induced by TGF-β1. Most importantly, we used an analytical docking experiment and thermal shift assay to further verify that NIF functions in conjunction with signal transducer and activator of transcription 3 (Stat3). Moreover, NIF inhibited the TGF-β/Smad pathway in vitro and decreased the expression of phosphorylated Stat3 in vitro and in vivo.
conclusionTaken together, we conclude that NIF inhibits and reverses pulmonary fibrosis, and these results support NIF as a viable therapeutic option for IPF treatment.
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