ArticleInternational journal of molecular sciences2020
Dimethyl Fumarate Attenuates Lung Inflammation and Oxidative Stress Induced by Chronic Exposure to Diesel Exhaust Particles in Mice.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Dimethyl fumarate as a versatile therapeutic agent: molecular mechanisms and potential clinical applications.Molecular biology reports · 2026Review
- Dimethyl Fumarate vs. Monomethyl Fumarate: Unresolved Pharmacologic Issues.Pharmaceutics · 2025Review
- Ferroptosis in Autoimmune Diseases: Research Advances and Therapeutic Strategies.International journal of molecular sciences · 2025Review
- Modulation of Pulmonary Inflammation and the Redox Pathway In Vitro and In Vivo by Fumaric Ester.Antioxidants (Basel, Switzerland) · 2025Article
- Exploring the Influence of Metabolic Changes in Fibrotic Lung Diseases.Pulmonary circulation · 2025Review
- Senotherapy for chronic lung disease.Pharmacological reviews · 2025Review
- Fumarate Hydratase Restrains mtDNA Attenuates LPS-Induced Acute Lung Injury Through cGAS-STING Pathways.Journal of inflammation research · 2025Article
- Reactive Oxygen Species in Asthma: Regulators of Macrophage Polarization and Therapeutic Implications: A Narrative Review.Journal of asthma and allergy · 2025Review
- Inhibitors of the NLRP3 inflammasome pathway as promising therapeutic candidates for inflammatory diseases (Review).International journal of molecular medicine · 2023Review
- Targeting Inflammation in Non-Small Cell Lung Cancer through Drug Repurposing.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Dimethyl Fumarate Attenuates Di-(2-Ethylhexyl) Phthalate-Induced Nephrotoxicity Through the Nrf2/HO-1 and NF-κB Signaling Pathways.Inflammation · 2023Article
- Novel potential pharmacological applications of dimethyl fumarate-an overview and update.Frontiers in pharmacology · 2023Review
- Overview of the Mechanisms of Oxidative Stress: Impact in Inflammation of the Airway Diseases.Antioxidants (Basel, Switzerland) · 2022Review
- Diesel exhaust particles distort lung epithelial progenitors and their fibroblast niche.Environmental pollution (Barking, Essex : 1987) · 2022Article
- Dimethyl fumarate ameliorates lipopolysaccharide-induced acute lung injury by inhibiting NLRP3 inflammasome-mediated pyroptosis through enhancing Nrf2 signaling.Toxicology research · 2022Article
- Dimethyl Fumarate Ameliorates Doxorubicin-Induced Cardiotoxicity By Activating the Nrf2 Pathway.Frontiers in pharmacology · 2022Article
- Dimethyl fumarate prevents acute lung injury related cognitive impairment potentially via reducing inflammation.Journal of cardiothoracic surgery · 2021Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Air pollution is mainly caused by burning of fossil fuels, such as diesel, and is associated with increased morbidity and mortality due to adverse health effects induced by inflammation and oxidative stress. Dimethyl fumarate (DMF) is a fumaric acid ester and acts as an antioxidant and anti-inflammatory agent. We investigated the potential therapeutic effects of DMF on pulmonary damage caused by chronic exposure to diesel exhaust particles (DEPs). Mice were challenged with DEPs (30 μg per mice) by intranasal instillation for 60 consecutive days. After the first 30 days, the animals were treated daily with 30 mg/kg of DMF by gavage for the remainder of the experimental period. We demonstrated a reduction in total inflammatory cell number in the bronchoalveolar lavage (BAL) of mice subjected to DEP + DMF as compared to those exposed to DEPs alone. Importantly, DMF treatment was able to reduce lung injury caused by DEP exposure. Intracellular total reactive oxygen species (ROS), peroxynitrite (OONO), and nitric oxide (NO) levels were significantly lower in the DEP + DMF than in the DEP group. In addition, DMF treatment reduced the protein expression of kelch-like ECH-associated protein 1 (Keap-1) in lung lysates from DEP-exposed mice, whereas total nuclear factor κB (NF-κB) p65 expression was decreased below baseline in the DEP + DMF group compared to both the control and DEP groups. Lastly, DMF markedly reduced DEP-induced expression of nitrotyrosine, glutathione peroxidase-1/2 (Gpx-1/2), and catalase in mouse lungs. In summary, DMF treatment effectively reduced lung injury, inflammation, and oxidative and nitrosative stress induced by chronic DEP exposure. Consequently, it may lead to new therapies to diminish lung injury caused by air pollutants.
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