Corpus ID: 20141477

The anti-inflammatory mechanism of sulfasalazine is related to adenosine release at inflamed sites.

  title={The anti-inflammatory mechanism of sulfasalazine is related to adenosine release at inflamed sites.},
  author={Pratap Gadangi and M Longaker and Dwight Naime and Richard I. Levin and Phoebe A. Recht and Mar{\'i}a Carmen Montesinos and M T Buckley and G Carlin and B N Cronstein},
  journal={Journal of immunology},
  volume={156 5},
The anti-inflammatory mechanism of sulfasalazine is not well understood. It has recently been shown that sulfasalazine inhibits 5-aminoimidazole-4-carboxamidoribonucleotide (AICAR) transformylase, an enzyme involved in de novo purine biosynthesis. We recently demonstrated that methotrexate promotes intracellular AICAR accumulation, thereby increasing adenosine release and diminishing inflammation, so we tested the hypothesis that sulfasalazine similarly promotes intracellular AICAR accumulation… Expand
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The growing evidence is outlined to support the hypothesis that the development of agonists selective for the A2A receptor is an effective strategy for suppressing the exaggerated inflammatory responses associated with many diseases by virtue of the receptor's ability to inhibit multiple pro‐inflammatory signalling cascades. Expand
Methotrexate and sulfasalazine promote adenosine release by a mechanism that requires ecto-5'-nucleotidase-mediated conversion of adenine nucleotides.
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Antinociceptive and anti-inflammatory properties of an adenosine kinase inhibitor and an adenosine deaminase inhibitor.
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Adenosine A2A or A3 receptors are required for inhibition of inflammation by methotrexate and its analog MX-68.
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Treatment with sulfasalazine or sulfapyridine, but not 5-aminosalicyclic acid, inhibits basic fibroblast growth factor-induced endothelial cell chemotaxis.
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