ArticleBritish journal of pharmacology2001
Apocynin and 1400 W prevents airway hyperresponsiveness during allergic reactions in mice.
Article in British journal of pharmacology, 2001. 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, 50 citations in OpenAlex.
- Thiol redox chemistry: role of protein cysteine oxidation and altered redox homeostasis in allergic inflammation and asthma.Journal of cellular biochemistry · 2015Review
- Anti-inflammatory effects of methoxyphenolic compounds on human airway cells.Journal of inflammation (London, England) · 2012Article
- Apocynin improves insulin resistance through suppressing inflammation in high-fat diet-induced obese mice.Mediators of inflammation · 2010Article
- Arginase: a key enzyme in the pathophysiology of allergic asthma opening novel therapeutic perspectives.British journal of pharmacology · 2009Review
- 4-Hydr-oxy-3-meth-oxy-5-nitro-aceto-phenone (5-nitro-apocynin).Acta crystallographica. Section E, Structure reports online · 2009Article
- Arginase and pulmonary diseases.Naunyn-Schmiedeberg's archives of pharmacology · 2008Review
- Apocynin: molecular aptitudes.Mediators of inflammation · 2008Review
- Asymmetric dimethylarginine induces oxidative and nitrosative stress in murine lung epithelial cells.American journal of respiratory cell and molecular biology · 2007Article
- Nonhematopoietic NADPH oxidase regulation of lung eosinophilia and airway hyperresponsiveness in experimentally induced asthma.American journal of physiology. Lung cellular and molecular physiology · 2007Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. The contribution of reactive nitrogen species to the development of airway hyperresponsiveness in a mouse model of allergic inflammation was investigated by the use of selective inhibitors of nitric oxide and superoxide formation. 2. Sensitized mice, repeatedly challenged with ovalbumin showed a significant (P<0.001, n=9) increase in airway responsiveness measured using whole body plethysmography. This hyperresponsiveness was accompanied by an influx of eosinophils into the airway lumen and increased levels of ovalbumin-specific serum IgE. 3. Treatment of mice with the iNOS inhibitor 1400 W or the NADPH-oxidase inhibitor apocynin did not significantly alter cellular influx into the airway lumen nor serum ovalbumin specific IgE. In contrast, apocynin as well as 1400 W inhibited ovalbumin-induced airway hyperresponsiveness (P<0.001 and P<0.05 respectively, n=9). Furthermore, the airways of allergen challenged animals showed clear 3-nitrotyrosine staining, which was mainly located in eosinophils. Remarkably, treatment with apocynin or 1400 W did not alter 3-nitrotyrosine staining. 4. These data suggest that the development of airway hyperresponsiveness during the airway inflammation upon ovalbumin challenge is dependent on the release of both superoxide and nitric oxide and is therefore likely to be dependent on reactive nitrogen species. This mechanism, however, is not reflected by 3-nitrotyrosine formation in the airways.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.