Abstract
The role of the adenosine A3 receptor (A3AR) in experimental colitis is controversial. The A3AR agonist N(6)-(3-iodobenzyl)adenosine-5'-N-methyluronamide (IB-MECA) has been shown to have a clinical benefit, although studies in A3AR-deficient mice suggest a pro-inflammatory role. However, there are no studies on the effect of 2-Cl-IB-MECA and the molecular mechanism of action of A3AR in murine colitis models in vivo. Is it the same as that observed in vitro? The interaction between 2-CL-IB-MECA and A3AR in a murine colitis model and the signaling pathways associated with this interaction remain unclear. Here we demonstrate a role for the NF-κB signaling pathway and its effect on modifying the activity of proinflammatory factors in A3AR-mediated biological processes. Our results demonstrated that A3AR activation possessed marked effects on experimental colitis through the NF-κB signaling pathway.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adenosine / administration & dosage
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Adenosine / analogs & derivatives
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Adenosine / pharmacology
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Adenosine A3 Receptor Agonists / administration & dosage
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Adenosine A3 Receptor Agonists / pharmacology*
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Animals
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Colitis / chemically induced
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Colitis / drug therapy
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Colitis / metabolism*
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Colitis / pathology
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Cytokines / genetics
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Cytokines / metabolism
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Disease Models, Animal
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Gene Expression
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Inflammation Mediators / metabolism
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Intestinal Mucosa / drug effects
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Intestinal Mucosa / metabolism
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Intestinal Mucosa / pathology
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Mice
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NF-kappa B / metabolism*
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Peroxidase / metabolism
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Receptor, Adenosine A3 / genetics
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Receptor, Adenosine A3 / metabolism*
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Signal Transduction / drug effects*
Substances
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Adenosine A3 Receptor Agonists
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Cytokines
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Inflammation Mediators
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NF-kappa B
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Receptor, Adenosine A3
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Peroxidase
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Adenosine
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2-chloro-N(6)-(3-iodobenzyl)adenosine-5'-N-methyluronamide