title: The adenosine A2A receptor agonist CGS 21680 fails to ameliorate the course of dextran sulphate-induced colitis in mice.
abstract: OBJECTIVE
  In this study we investigated the effect of CGS 21680 (2-p-(2-Carboxyethyl)phenethylamino-5-N-ethylcarboxamidoadenosine hydrochloride), an adenosine A2A receptor agonist, in a model of dextran sulphate sodium (DSS)-induced colitis.
  
  
  METHODS
  NMRI mice were fed 5 % (w/v) DSS, and were treated intraperitoneally with 0.5 mg/kg CGS 21680 or vehicle for 10 days. Changes of bodyweight, colon length, the incidence of rectal bleeding, levels of macrophage inflammatory protein (MIP)-1alpha, MIP-2, interferon gamma, interleukin (IL)-1beta, IL-12 and tumour necrosis factor-alpha from homogenates of colon biopsies, and the release of [3H]acetylcholine (ACh) from longitudinal muscle strip were determined.
  
  
  RESULTS
  DSS significantly decreased bodyweight, colon length, and it increased the incidence of rectal bleeding and levels of MIP-1alpha, MIP-2 and IL-1beta compared to DSS-untreated animals. CGS 21680 had no effect on these changes. No change could be observed in release of ACh in DSS-induced colitis with or without CGS 21680.
  
  
  CONCLUSIONS
  In summary, CGS 21680 is ineffective in ameliorating DSS-induced colitis in mice.
authors.affiliation: Department of Pharmacology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, Hungary. selmeczy@koki.hu
authors.forename: Z
authors.initials: Z
authors.lastname: Selmeczy
authors.forename: B
authors.initials: B
authors.lastname: Csóka
authors.forename: P
authors.initials: P
authors.lastname: Pacher
authors.forename: E S
authors.initials: ES
authors.lastname: Vizi
authors.forename: G
authors.initials: G
authors.lastname: Haskó
mesh_terms: D000109:Acetylcholine / Q000235:genetics / Q000378:metabolism; D000241:Adenosine / Q000031:analogs & derivatives* / Q000627:therapeutic use; D058908:Adenosine A2 Receptor Agonists; D000818:Animals; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D054426:Chemokine CXCL2; D018925:Chemokines / Q000235:genetics / Q000378:metabolism; D003092:Colitis / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism; D016264:Dextran Sulfate; D005786:Gene Expression Regulation / Q000187:drug effects; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism; D019402:Macrophage Inflammatory Proteins / Q000235:genetics / Q000378:metabolism; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains / Q000502:physiology; D009130:Muscle, Smooth / Q000378:metabolism / Q000473:pathology; D010627:Phenethylamines / Q000627:therapeutic use*
chemical_list: D058908:Adenosine A2 Receptor Agonists; D000959:Antihypertensive Agents; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D054426:Chemokine CXCL2; D018925:Chemokines; C404915:Cxcl2 protein, mouse; D053583:Interleukin-1beta; D019402:Macrophage Inflammatory Proteins; D010627:Phenethylamines; C061282:2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosine; D016264:Dextran Sulfate; D000241:Adenosine; D000109:Acetylcholine