ArticleInternational journal of molecular sciences2023
Inhibition of Fatty Acid Amide Hydrolase (FAAH) Regulates NF-kb Pathways Reducing Bleomycin-Induced Chronic Lung Inflammation and Pulmonary Fibrosis.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 5 citations in OpenAlex.
- Ginseng as a Functional Food Intervention for Interstitial Lung Disease: A Review of the Benefits and Molecular Mechanisms.Food science & nutrition · 2026Review
- Isoforskolin inhibits LUBAC/GSDMD/IL-1β cascades in pulmonary fibrosis.Journal of thoracic disease · 2026Article
- Special Issue "New Perspective in the Molecular Pathways Involved in Acute and Chronic Lung Injury".International journal of molecular sciences · 2025Article
- Hyaluronic Acid-Decorated Liposomes for the Intrapulmonary Delivery of Imatinib: A Targeted Treatment for Postinflammatory Pulmonary Fibrosis.Small science · 2025Article
- Molecular Mechanism of Action of Endocrine-Disrupting Chemicals on the Respiratory System.International journal of molecular sciences · 2024Review
- Piperine alleviates nonalcoholic steatohepatitis by inhibiting NF-κB-mediated hepatocyte pyroptosis.PloS one · 2024Article
- FAAH inhibition ameliorates breast cancer in a murine model.Oncotarget · 2023Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The deadly interstitial lung condition known as idiopathic pulmonary fibrosis (IPF) worsens over time and for no apparent reason. The traditional therapy approaches for IPF, which include corticosteroids and immunomodulatory drugs, are often ineffective and can have noticeable side effects. The endocannabinoids are hydrolyzed by a membrane protein called fatty acid amide hydrolase (FAAH). Increasing endogenous levels of endocannabinoid by pharmacologically inhibiting FAAH results in numerous analgesic advantages in a variety of experimental models for pre-clinical pain and inflammation. In our study, we mimicked IPF by administering intratracheal bleomycin, and we administered oral URB878 at a dose of 5 mg/kg. The histological changes, cell infiltration, pro-inflammatory cytokine production, inflammation, and nitrosative stress caused by bleomycin were all reduced by URB878. Our data clearly demonstrate for the first time that the inhibition of FAAH activity was able to counteract not only the histological alteration bleomycin-induced but also the cascade of related inflammatory events.
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Registered trials
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