• Tianhua Ren, Ting Tian, Xiao Feng, Shicai Ye, Hao Wang, Weiyun Wu, Yumei Qiu, Caiyuan Yu, Yanting He, Juncheng Zeng, Junwei Cen, and Yu Zhou.
• Department of Gastroenterology, The Affiliated Hospital of Guangdong Medical College, No. 57 South Renmin Avenue, Zhanjiang 524001, China.
• Sci Rep. 2015 Jan 1; 5: 9047.

AbstractThe 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.

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