Abstract
BackgroundEndothelial 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.MethodsWe 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.ResultsMAdCAM-1 was induced by TNF-a. Melatonin at concentrations over 100 μm (10-4 M) significantly attenuated MAdCAM-1 expression and was maximal at 1 mM.ConclusionsOur data indicate that melatonin may exert therapeutic activity in IBD through its ability to inhibit NF-kB dependent induction of MAdCAM-1.
Highlights
IntroductionEndothelial MAdCAM-1 (mucosal addressin cell adhesion molecule-1) expression is associated with the oxidant-dependent induction and progress of inflammatory bowel disease (IBD)
Endothelial MAdCAM-1 expression is associated with the oxidant-dependent induction and progress of inflammatory bowel disease (IBD)
We have previously described that several therapeutic agents which are currently used for IBD therapy attenuate MAdCAM-1 expression and may explain part of the basis of therapy with these agents [7]
Summary
Endothelial MAdCAM-1 (mucosal addressin cell adhesion molecule-1) expression is associated with the oxidant-dependent induction and progress of inflammatory bowel disease (IBD). We have previously described that several therapeutic agents which are currently used for IBD therapy (dexamethasone, IL-10) attenuate MAdCAM-1 expression and may explain part of the basis of therapy with these agents [7]. Based on these results, we wished to determine if melatonin could have a significant impact on the expression of MAdCAM-1 in lymphatic endothelial cells that have been stimulated with TNF-a, and whether TNFa induced NF-kB activation in lymphatic endothelium is reduced by MAdCAM-1
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