ArticlePloS one2012
The JNK inhibitor XG-102 protects against TNBS-induced colitis.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 47 citations in OpenAlex.
- Antisense inhibition of RNA polymerase α subunit ofMicrobiology spectrum · 2023Article
- Protection by microRNA-7a-5p Antagomir Against Intestinal Mucosal Injury Related to the JNK Pathway in TNBS-Induced Experimental Colitis.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2021Article
- Visfatin Regulates Inflammatory Mediators in Mouse Intestinal Mucosa Through Toll-Like Receptors Signaling Under Lipopolysaccharide Stress.Archivum immunologiae et therapiae experimentalis · 2021Article
- c-Jun N-Terminal Kinase Inhibitors as Potential Leads for New Therapeutics for Alzheimer's Diseases.International journal of molecular sciences · 2020Review
- Berberine Suppresses Colonic Inflammation in Dextran Sulfate Sodium-Induced Murine Colitis Through Inhibition of Cytosolic Phospholipase A2 Activity.Frontiers in pharmacology · 2020Article
- The Impact of Chronic Intestinal Inflammation on Brain Disorders: the Microbiota-Gut-Brain Axis.Molecular neurobiology · 2019Review
- Local level of TGF-β1 determines the effectiveness of dexamethasone through regulating the balance of Treg/Th17 cells in TNBS-induced mouse colitis.Experimental and therapeutic medicine · 2018Article
- c-Jun N-terminal kinase 2 promotes enterocyte survival and goblet cell differentiation in the inflamed intestine.Mucosal immunology · 2017Article
- Investigation of the relationship between the Th17/IL-23 pathway and innate-adaptive immune system in TNBS-induced colitis in rats.Iranian journal of basic medical sciences · 2017Article
- Role of C-Jun N-terminal Kinase in Hepatocellular Carcinoma Development.Targeted oncology · 2016Review
- Modulation of c-Jun N-terminal kinase signaling and specific glucocorticoid receptor phosphorylation in the treatment of major depression.Medical hypotheses · 2015Article
- Article
- Gadolinium chloride improves the course of TNBS and DSS-induced colitis through protecting against colonic mucosal inflammation.Scientific reports · 2014Article
- Jnk2 deletion disrupts intestinal mucosal homeostasis and maturation by differentially modulating RNA-binding proteins HuR and CUGBP1.American journal of physiology. Cell physiology · 2014Article
- XG-102 administered to healthy male volunteers as a single intravenous infusion: a randomized, double-blind, placebo-controlled, dose-escalating study.Pharmacology research & perspectives · 2014Article
- Resveratrol modulates cytokine-induced Jak/STAT activation more efficiently than 5-aminosalicylic acid: an in vitro approach.PloS one · 2014Article
- Hyperthermia differently affects connexin43 expression and gap junction permeability in skeletal myoblasts and HeLa cells.Mediators of inflammation · 2014Article
- JNK1 stress signaling is hyper-activated in high breast density and the tumor stroma: connecting fibrosis, inflammation, and stemness for cancer prevention.Cell cycle (Georgetown, Tex.) · 2014Article
- JNK signalling in cancer: in need of new, smarter therapeutic targets.British journal of pharmacology · 2014Review
- Repeated H2 O2 exposure drives cell cycle progression in an in vitro model of ulcerative colitis.Journal of cellular and molecular medicine · 2013Article
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The c-Jun N-terminal kinase (JNK)-inhibiting peptide D-JNKI-1, syn. XG-102 was tested for its therapeutic potential in acute inflammatory bowel disease (IBD) in mice. Rectal instillation of the chemical irritant trinitrobenzene sulfonic acid (TNBS) provoked a dramatic acute inflammation in the colon of 7-9 weeks old mice. Coincident subcutaneous application of 100 µg/kg XG-102 significantly reduced the loss of body weight, rectal bleeding and diarrhoea. After 72 h, the end of the study, the colon was removed and immuno-histochemically analysed. XG-102 significantly reduced (i) pathological changes such as ulceration or crypt deformation, (ii) immune cell pathology such as infiltration and presence of CD3- and CD68-positive cells, (iii) the production of tumor necrosis factor (TNF)-α in colon tissue cultures from TNBS-treated mice, (iv) expression of Bim, Bax, FasL, p53, and activation of caspase 3, (v) complexation of JNK2 and Bim, and (vi) expression and activation of the JNK substrate and transcription factor c-Jun. A single application of subcutaneous XG-102 was at least as effective or even better depending on the outcome parameter as the daily oral application of sulfasalazine used for treatment of IBD.The successful and substantial reduction of the severe, TNBS-evoked intestinal damages and clinical symptoms render the JNK-inhibiting peptide XG-102 a powerful therapeutic principle of IBD.
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