ArticleJournal of inflammation research2013
The impact of JNK inhibitor D-JNKI-1 in a murine model of chronic colitis induced by dextran sulfate sodium.
Article in Journal of inflammation research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
- Attack of the kinases: JNK signaling in metabolism.American journal of physiology. Regulatory, integrative and comparative physiology · 2026Review
- TNFSF14 (LIGHT) in intestinal inflammation: balancing immune activation and resolution in IBD.Frontiers in immunology · 2025Review
- Colocalization and Interaction Study of Neuronal JNK3, JIP1, and β-Arrestin2 Together with PSD95.International journal of molecular sciences · 2022Article
- Advances in Immunosuppressive Agents Based on Signal Pathway.Frontiers in pharmacology · 2022Review
- The lipid peroxidation product EKODE exacerbates colonic inflammation and colon tumorigenesis.Redox biology · 2021Article
- Cardiolipin-mediated PPARγ S112 phosphorylation impairs IL-10 production and inflammation resolution during bacterial pneumonia.Cell reports · 2021Article
- Article
- Selective inhibitors for JNK signalling: a potential targeted therapy in cancer.Journal of enzyme inhibition and medicinal chemistry · 2020Review
- Epigenetic histone modulation contributes to improvements in inflammatory bowel disease via EBI3.Cellular and molecular life sciences : CMLS · 2020Article
- c-Jun NH2-terminal kinase suppression significantly inhibits the growth of transplanted breast tumors in mice.The Journal of international medical research · 2020Article
- Anti-Inflammatory Effect of IL-37-Producing T-Cell Population in DSS-Induced Chronic Inflammatory Bowel Disease in Mice.International journal of molecular sciences · 2018Article
- Impaired resolution of DSS-induced colitis in mice lacking the glucocorticoid receptor in myeloid cells.PloS one · 2018Article
- Role of pregnane X-receptor in regulating bacterial translocation in chronic liver diseases.World journal of hepatology · 2017Review
- c-Jun N-terminal kinase 2 promotes enterocyte survival and goblet cell differentiation in the inflamed intestine.Mucosal immunology · 2017Article
- Therapeutic potential of tonsil-derived mesenchymal stem cells in dextran sulfate sodium-induced experimental murine colitis.PloS one · 2017Article
- Role of C-Jun N-terminal Kinase in Hepatocellular Carcinoma Development.Targeted oncology · 2016Review
- Pregnane X Receptor Activation Attenuates Inflammation-Associated Intestinal Epithelial Barrier Dysfunction by Inhibiting Cytokine-Induced Myosin Light-Chain Kinase Expression and c-Jun N-Terminal Kinase 1/2 Activation.The Journal of pharmacology and experimental therapeutics · 2016Article
- Molecular mechanism of protopanaxadiol saponin fraction-mediated anti-inflammatory actions.Journal of ginseng research · 2015Article
- Resveratrol modulates cytokine-induced Jak/STAT activation more efficiently than 5-aminosalicylic acid: an in vitro approach.PloS one · 2014Article
- JNK signalling in cancer: in need of new, smarter therapeutic targets.British journal of pharmacology · 2014Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeThe c-Jun N-terminal kinases (JNK) are involved in the activation of T cells and the synthesis of proinflammatory cytokines. Several studies have established the relevance of the JNK pathway in inflammatory bowel diseases. The present study analyzed the therapeutic effect of D-JNKI-1, a specific JNK-inhibiting peptide, in a low-dose dextran sulfate sodium (DSS) model of chronic colitis.
methodsDSS colitis was induced in female C57/BL6 mice by cyclic administration using different concentrations of DSS (1.0% and 1.5%). Mice in the intervention groups received subcutaneous administration of 1 μg/kg D-JNKI-1 on days 2, 12, and 22. They were monitored daily to assess the severity of colitis, body weight, stool consistency, and the occurrence of occult blood or gross rectal bleeding using evaluation of the disease activity index. The animals were sacrificed after 30 days, and the inflamed intestine was histologically evaluated using a crypt damage score. Immunohistochemical quantification of CD4(+) and CD8(+) cells was also carried out.
resultsAdministration of 1 μg/kg D-JNKI-1 resulted in a significant decrease in the disease activity index (P = 0.013 for 1.0% DSS; P = 0.007 for 1.5% DSS). As a mild form of colitis was induced, histological examination did not show any distinct damage to the mucosa and crypts. However, expression of CD4(+) and CD8(+) cells was reduced in mice treated with D-JNKI-1 (not significant).
conclusionAdministration of D-JNKI-1 resulted in a clinical attenuation of chronic DSS colitis, and a therapeutic effect of D-JNKI-1 must therefore be assumed. The decrease in CD4(+) and CD8(+) cells may reflect the influence of D-JNKI-1 on T-cell activation, differentiation, and migration.
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