An adenosine A3 receptor agonist inhibits DSS-induced colitis in mice through modulation of the NF-κB signaling pathway
Copyright policy )An adenosine A3 receptor agonist inhibits DSS-induced colitis in mice through modulation of the NF-κB signaling pathway
AbstractThe role of the adenosine A3 receptor (A3AR) in experimental colitis is controversial. The A3AR agonist N6-(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.
- Guangdong Medical College China (People's Republic of)
- Affiliated Hospital of Guangdong Medical College Hospital China (People's Republic of)
Adenosine, Receptor, Adenosine A3, NF-kappa B, Gene Expression, Colitis, Article, Disease Models, Animal, Mice, Adenosine A3 Receptor Agonists, Animals, Cytokines, Inflammation Mediators, Intestinal Mucosa, Peroxidase, Signal Transduction
Adenosine, Receptor, Adenosine A3, NF-kappa B, Gene Expression, Colitis, Article, Disease Models, Animal, Mice, Adenosine A3 Receptor Agonists, Animals, Cytokines, Inflammation Mediators, Intestinal Mucosa, Peroxidase, Signal Transduction
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