{"@type": "dcat:Dataset", "accessLevel": "public", "bureauCode": ["009:25"], "contactPoint": {"@type": "vcard:Contact", "fn": "NIH", "hasEmail": "mailto:info@nih.gov"}, "description": "Background\n          Endothelial MAdCAM-1 (mucosal addressin cell adhesion molecule-1) expression is associated with the oxidant-dependent induction and progress of inflammatory bowel disease (IBD). Melatonin, a relatively safe, potent antioxidant, has shown efficacy in several chronic injury models may limit MAdCAM-1 expression and therefore have a therapeutic use in IBD.\n        \n        \n          Methods\n          We examined how different doses of melatonin reduced endothelial MAdCAM-1 induced by TNF-a in an in vitro model of lymphatic endothelium. Endothelial monolayers were pretreated with melatonin prior to, and during an exposure, to TNF-a (1 ng/ml, 24 h), and MAdCAM-1 expression measured by immunoblotting.\n        \n        \n          Results\n          MAdCAM-1 was induced by TNF-a. Melatonin at concentrations over 100 \u03bcm (10-4 M) significantly attenuated MAdCAM-1 expression and was maximal at 1 mM.\n        \n        \n          Conclusions\n          Our data indicate that melatonin may exert therapeutic activity in IBD through its ability to inhibit NF-kB dependent induction of MAdCAM-1.", "distribution": [{"@type": "dcat:Distribution", "description": "Visit the original government dataset for complete information, documentation, and data access.", "downloadURL": "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC111062/", "mediaType": "text/html", "title": "Official Government Data Source"}], "identifier": "https://healthdata.gov/api/views/8h8t-4czt", "issued": "2025-07-14", "keyword": ["inflammatory-bowel-disease", "madcam-1-expression", "melatonin-treatment", "nih", "tnf-alpha"], "landingPage": "https://healthdata.gov/d/8h8t-4czt", "modified": "2025-09-06", "programCode": ["009:033"], "publisher": {"@type": "org:Organization", "name": "National Institutes of Health"}, "theme": ["NIH"], "title": "Melatonin reduces TNF-a induced expression of MAdCAM-1 via inhibition of NF-kB."}