ArticleImmunology2004
Effect of an inhibitor of Jun N-terminal protein kinase, SP600125, in single allergen challenge in sensitized rats.
Article in Immunology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 44 citations in OpenAlex.
- Leonurine Exerts an Anti-Primary Dysmenorrhea Effect in Rats by Inactivating the JNK/p38 Pathway.Applied biochemistry and biotechnology · 2026Article
- Histamine HInternational journal of molecular sciences · 2024Article
- Anti-oxidant and Anti-inflammatory Effects of Aquatic Exercise in Allergic Airway Inflammation in Mice.Frontiers in physiology · 2019Article
- Role of C-Jun N-terminal Kinase in Hepatocellular Carcinoma Development.Targeted oncology · 2016Review
- TSG-6 secreted by human umbilical cord-MSCs attenuates severe burn-induced excessive inflammation via inhibiting activations of P38 and JNK signaling.Scientific reports · 2016Article
- Absence of c-Jun NH2-terminal kinase 1 protects against house dust mite-induced pulmonary remodeling but not airway hyperresponsiveness and inflammation.American journal of physiology. Lung cellular and molecular physiology · 2014Article
- TEC and MAPK Kinase Signalling Pathways in T helper (TJournal of clinical & cellular immunology · 2012Article
- c-Jun N-terminal kinase 1 is required for the development of pulmonary fibrosis.American journal of respiratory cell and molecular biology · 2009Article
- Shift work and pathological conditions.Journal of occupational medicine and toxicology (London, England) · 2006Article
- Mitogen activated protein kinase inhibitors: where are we now and where are we going?Annals of the rheumatic diseases · 2006Review
- Differences in MAP kinase phosphorylation in response to mechanical strain in asthmatic fibroblasts.Respiratory research · 2006Article
- Chronic cough due to occupational factors.Journal of occupational medicine and toxicology (London, England) · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Jun N-terminal kinase (JNK) has been implicated in the pathogenesis of inflammatory diseases including asthma. We examined the effect of SP600125 (anthra [1,9-cd] pyrazol-6 (2H)-one), a novel inhibitor of JNK in a model of asthma. Brown-Norway rats were sensitized to ovalbumin and treated with SP600125 intraperitoneally (90 mg/kg in total). SP600125 inhibited allergen-induced, increased activity of phosphorylated c-jun but not of phosphorylated-MAPKAPK2, indicative of activation of p38 MAPK, in the lung. SP600125 inhibited macrophage (P < 0.04), lymphocyte (P < 0.05), eosinophil (P < 0.04) and neutrophil (P < 0.005) numbers in bronchoalveolar lavage. Eosinophil and T-cell accumulation in the airways, mRNA expression for interleukin-1beta, tumour necrosis factor-beta, interleukin-3, interleukin-4 and interleukin-5, serum levels of allergen-specific immunoglobulin E and bronchial hyperresponsiveness were not affected by SP600125. Selective inhibition of JNK reduced inflammatory cell egress into the airway lumen after single allergen exposure. The role of JNK mitogen-activated protein kinase activation may be limited in the pathogenesis of bronchial hyperresponsiveness after single allergen exposure.
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What OpenQuestion holds
Registered trials
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.