0000000000672796

AUTHOR

U. Mittelkötter

showing 3 related works from this author

Genetic Deletion of JNK1 and JNK2 Aggravates the DSS-Induced Colitis in Mice

2007

The c-Jun N-terminal kinases (JNKs) are considered as novel targets for therapy of inflammatory bowel diseases (IBD). However, the relevant JNK isoforms have to be elucidated. Here, we analyze the individual contribution of the JNK1 and JNK2 isoforms in a dextran sulfate sodium (DSS) model of experimental colitis. JNK1 and JNK2 knockout mice (JNK1 ko, JNK2 ko) and their wild-type controls (WT1, WT2) received three cycles of DSS treatment, each consisting of 1.7% DSS for 5 days, followed by 5 days with water. Animals were daily evaluated by a disease activity index (DAI) comprising measurement of body weight, estimation of stool consistency, and test for occult blood/gross rectal bleeding. A…

medicine.medical_specialtyPathologyCryptApoptosisMice TransgenicInflammatory bowel diseaseGastroenterologyProinflammatory cytokineMiceCecumImmune systemInternal medicineWeight LossAnimalsMitogen-Activated Protein Kinase 9MedicineMitogen-Activated Protein Kinase 8Single-Blind MethodIntestinal MucosaColitisCrosses Geneticbusiness.industryDextran SulfateColitismedicine.diseaseMice Inbred C57BLmedicine.anatomical_structureApoptosisChronic DiseaseKnockout mouseSurgeryGastrointestinal HemorrhagebusinessJournal of Investigative Surgery
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Oral administration of taurolidine ameliorates chronic DSS colitis in mice.

2007

Taurolidine (TRD) has antimicrobial and anti-inflammatory properties. However, the anti-inflammatory effects of TRD in inflammatory bowel diseases (IBD) have not been investigated. Here, we have analyzed the toxicity of TRD after oral long-term application in mice and examined the impact of oral TRD in a dextran sulfate sodium (DSS) model of experimental colitis. Female C57/BL6 mice received TRD in various concentrations (0.1% to 0.4%) for 60 days. Toxicity was evaluated by use of a disease activity index (DAI) and histological examination of major metabolic organs. Furthermore, the impact of 0.2% TRD on a chronic DSS colitis was examined by daily DAI, histological crypt damage score (CDS),…

medicine.medical_specialtyColonTaurineAdministration OralGastroenterologyInflammatory bowel diseasechemistry.chemical_compoundMiceOral administrationInternal medicinemedicineMesenteric lymph nodesAnimalsColitisThiadiazinesbusiness.industryDextran SulfateInterleukinTaurolidinemedicine.diseaseColitisInflammatory Bowel DiseasesMice Inbred C57BLmedicine.anatomical_structurechemistryCyclooxygenase 2Bacterial TranslocationImmunologyToxicityCytokinesSurgeryTumor necrosis factor alphaFemaleLymph NodesbusinessJournal of investigative surgery : the official journal of the Academy of Surgical Research
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Knock out der c-Jun N-terminalen Kinase 2 (JNK2) aggraviert die Entwicklung der chronischen DSS-Colitis unabhängig von der intestinalen Zytokin-Expre…

2008

Background The c-Jun N-terminal kinase 2 (JNK2) is involved in signal transduction of inflammatory bowel diseases (IBD) and regulates the expression of pro-inflammatory cytokines. For this reason, JNK2 is considered as novel target for IBD therapy. The aim of this study was 1.) to examine the function of JNK2 applying a low dose Dextran Sulfate Sodium (DSS) model of chronic experimental colitis in JNK2 knock out mice and 2.) to analyze the expression of JNK2 dependent cytokines. Material and Methods: For induction of a mild chronic colitis, female JNK2 knockout mice (JNK2 ko) and their wildtype controls (WT2) received three cycles of DSS treatment, each consisting of 1.0 % DSS for 5 days, f…

business.industryKinaseCryptWild typeInflammationmedicine.diseaseAndrologyImmune systemddc: 610Knockout mousemedicineTumor necrosis factor alphamedicine.symptomColitisbusiness
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