An adenosine A3 receptor agonist inhibits DSS-induced colitis in mice through modulation of the NF-[kappa]B signaling pathway

The 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 a...

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Bibliographic Details
Published in:Scientific reports 2015-03, Vol.5, p.9047
Main Authors: Ren, Tianhua, Tian, Ting, Feng, Xiao, Ye, Shicai, Wang, Hao, Wu, Weiyun, Qiu, Yumei, Yu, Caiyuan, He, Yanting, Zeng, Juncheng, Cen, Junwei, Zhou, Yu
Format: Article
Language:English
Subjects:
Animal models
Colitis
Inflammation
Inflammatory bowel disease
Molecular modelling
NF-κB protein
Rodents
Signal transduction
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Summary:The 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.
ISSN:2045-2322
DOI:10.1038/srep09047