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.
An adenosine A3 receptor agonist inhibits DSS-induced colitis in mice through modulation of the NF-κB signaling pathway
Tian-hua Ren,Ting Tian,Xiao Feng,Shicai Ye,Weiyun Wu,Yumei Qiu,Cai-yuan Yu,Yanting He,Juncheng Zeng,Junwei Cen,Yu Zhou
Published 2015 in Scientific Reports
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- Publication year
2015
- Venue
Scientific Reports
- Publication date
2015-03-12
- Fields of study
Biology, Medicine
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Semantic Scholar, PubMed
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