Background: 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.
Methods: 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.
Results: MAdCAM-1 was induced by TNF-a. Melatonin at concentrations over 100 microm (10(-4) M) significantly attenuated MAdCAM-1 expression and was maximal at 1 mM.
Conclusions: Our data indicate that melatonin may exert therapeutic activity in IBD through its ability to inhibit NF-kappaB dependent induction of MAdCAM-1.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC111062 | PMC |
| http://dx.doi.org/10.1186/1471-230x-2-9 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Case report: Vedolizumab in Oral Crohn's disease: the downsides of a gut-specific therapy for a multi-site disease.
Front Med (Lausanne)
December 2024
Department of Oral Medicine, Royal London Hospital, Barts Health NHS Trust, London, United Kingdom.
Introduction: Crohn's disease (CD) is a chronic inflammatory bowel disease which can affect any area of the gastrointestinal tract, including oral tissues. The complex nature of this disease demands interdisciplinary management, especially when both intestinal and oral manifestations are present.
Case: This report presents the case of a 28-year-old male patient with oral, ileo-caecal and peri-anal CD managed jointly between Gastroenterology and Oral Medicine.
Mucosal Addressin Cell Adhesion Molecule-1 Mediates T Cell Migration into Pancreas-Draining Lymph Nodes for Initiation of the Autoimmune Response in Type 1 Diabetes.
Int J Mol Sci
October 2024
Department of Pathology, School of Medicine, Stanford University, Stanford, CA 94305, USA.
Type 1 diabetes (T1D) is an autoimmune disease that is caused by autoreactive T cell-mediated destruction of insulin-producing β cells in the pancreatic islets. Although naive autoreactive T cells are initially primed by islet antigens in pancreas-draining lymph nodes (pan-LNs), the adhesion molecules that recruit T cells into pan-LNs are unknown. We show that high endothelial venules in pan-LNs of young nonobese diabetic mice have a unique adhesion molecule profile that includes strong expression of mucosal addressin cell adhesion molecule-1 (MAdCAM-1).
View Article and Find Full Text PDFFucoidan modulates gut microbiota and immunity in Peyer's patches against inflammatory bowel disease.
Carbohydr Polym
October 2024
Department of Biology, College of Science, Shantou University, Shantou 515063, Guangdong, China; Guangdong Provincial Key Laboratory of Aquatic Product Processing and Safety, College of Food Science and Technology, Guangdong Ocean University, Zhanjiang, China. Electronic address:
Although fucoidan has potential use as an anti-inflammatory agent, the specific mechanisms by which it influences signaling and immunomodulatory pathways between gut microbiota and Peyer's patches remain unclear. Therefore, the aim of this study was to investigate the therapeutic potential of fucoidan in a dextran sulfate sodium (DSS)-induced mouse model of inflammatory bowel disease (IBD) by examining the effects on gut microbiota and the underlying anti-inflammatory mechanisms. Purified fucoidan, which upon characterization revealed structural fragments comprising →3)-β-D-Galp-(1→, →4)-α-L-Fucp-(1→, and →3)-α-L-Fucp-(1→ residues with a sulfation at position C2 was used.
View Article and Find Full Text PDFmiR-200c-3p regulates α4 integrin-mediated T cell adhesion and migration.
Exp Cell Res
July 2024
Department of Molecular Pathobiology and Cell Adhesion Biology, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu, Mie 514-8507, Japan. Electronic address:
A microRNA miR-200c-3p is a regulator of epithelial-mesenchymal transition to control adhesion and migration of epithelial and mesenchymal cells. However, little is known about whether miR-200c-3p affects lymphocyte adhesion and migration mediated by integrins. Using TK-1 (a T lymphoblast cell) as a model of T cell, here we show that repressed expression of miR-200c-3p upregulated α4 integrin-mediated adhesion to and migration across mucosal addressin cell adhesion molecule-1 (MAdCAM-1).
View Article and Find Full Text PDFExploring the therapeutic potential of porphyran extracted from Porphyra haitanensis in the attenuation of DSS-induced intestinal inflammation.
Int J Biol Macromol
June 2024
Guangxi Key Laboratory of Beibu Gulf Biodiversity Conservation, Beibu Gulf University, Qinzhou, Guangxi, China. Electronic address:
Ulcerative colitis is a chronic, spontaneous inflammatory bowel disease that primarily affects the colon. This study aimed to explore how Porphyra haitanensis porphyran (PHP) modulates the immune response and the associated mechanisms that alleviate dextran sulphate sodium-induced colitis in mice. Histological assessments via H&E staining and AB-PAS staining revealed that PHP intervention partially restored the number of goblet cells and improved intestinal mucosal function.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!