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.
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Authors | Tianhua Ren, Ting Tian, Xiao Feng, Shicai Ye, Hao Wang, Weiyun Wu, Yumei Qiu, Caiyuan Yu, Yanting He, Juncheng Zeng, Junwei Cen, Yu Zhou |
Journal | Scientific reports
(Sci Rep)
Vol. 5
Pg. 9047
(Mar 12 2015)
ISSN: 2045-2322 [Electronic] England |
PMID | 25762375
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Adenosine A3 Receptor Agonists
- Cytokines
- Inflammation Mediators
- NF-kappa B
- Receptor, Adenosine A3
- Peroxidase
- Adenosine
- 2-chloro-N(6)-(3-iodobenzyl)adenosine-5'-N-methyluronamide
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Topics |
- Adenosine
(administration & dosage, analogs & derivatives, pharmacology)
- Adenosine A3 Receptor Agonists
(administration & dosage, pharmacology)
- Animals
- Colitis
(chemically induced, drug therapy, metabolism, pathology)
- Cytokines
(genetics, metabolism)
- Disease Models, Animal
- Gene Expression
- Inflammation Mediators
(metabolism)
- Intestinal Mucosa
(drug effects, metabolism, pathology)
- Mice
- NF-kappa B
(metabolism)
- Peroxidase
(metabolism)
- Receptor, Adenosine A3
(genetics, metabolism)
- Signal Transduction
(drug effects)
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