Abstract
Nociceptin/orphanin (Noc/oFQ), endogenous agonist for nociceptin receptor (NOR), is thought to be a stimulator of neurogenic inflammation. We investigated the possible role of Noc/oFQ in the development of colitis using NOR-deficient mice treated with dextran sulfate sodium (DSS). Colitis was significantly improved in NOR-deficient mice against wild-type mice. Expression level of mucosal addressin cell adhesion molecule-1 (MAdCAM-1) and infiltrating cells also significantly decreased in NOR-deficient mice against wild-type mice. Nociceptin expression increased in wild-type mice after DSS treatment. These results suggest stimulation by Noc/oFQ deteriorates colonic inflammation via up-regulation of adhesion molecule.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Antigens, CD / metabolism
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Body Weight / physiology
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Cell Adhesion Molecules / metabolism
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Cell Count / methods
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Colitis / chemically induced
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Colitis / genetics
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Colitis / metabolism*
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Colitis / pathology
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Colon / pathology
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Dextran Sulfate
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Disease Models, Animal*
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Female
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Gastric Mucosa / cytology
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Gastric Mucosa / metabolism
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Gastric Mucosa / pathology
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Gene Expression Regulation / drug effects
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Gene Expression Regulation / genetics
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Immunohistochemistry / methods
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Integrin beta Chains / metabolism
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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Mucoproteins
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Nociceptin
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Opioid Peptides / deficiency
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Opioid Peptides / physiology*
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Staining and Labeling / methods
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Time Factors
Substances
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Antigens, CD
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Cell Adhesion Molecules
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Integrin beta Chains
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Madcam1 protein, mouse
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Mucoproteins
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Opioid Peptides
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integrin beta7
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Dextran Sulfate