title: [CRTH2 antagonist ameliorates airway inflammation in rats with asthma].
abstract: To investigate the effect of prostaglandin D2 receptor antagonists on the airway inflammation in rats with asthma.
  
  
  
  Forty male SD rats were randomly divided into four groups: Group A (normal control), Group B (asthma group), Group C (CRTH2 antagonist BAYu3405 treatment group), Group D (DP1 antagonist BWA868C treatment group). Asthma was induced by ovalbumin (OVA) challenge. The rats in each group were sacrificed 24 h after the last challenge of OVA.DP1/CRTH2 receptors on eosinophils (EOS) were measured by radiological binding assay (RBA). The left lungs were used for histological examinations and bronchoalveolar lavage fluid (BALF) was collected from the right lungs. The total cell numbers, EOS absolute count and differential cell counts in BALF were performed. Serum concentrations of IL-4, 5 and IFN-gamma were measured by ELISA.
  
  
  
  Rats in BAYu3405 treatment group showed profoundly decreased infiltrates of EOS and lymphocytes in the wall of bronchus when compared with those of asthma group and BWA868C treatment group. Serum concentrations of IFN-gamma in rats of BAYu3405 treatment group increased, but IL-4 and IL-5 decreased significantly when compared with those in rats of asthma group and BWA868C treatment group (P<0.01), and BALF EOS count was decreased significantly (P<0.01). Peripheral blood EOS count was higher than that in rats of normal control group, but was not significantly different from that in rats of asthma group and BWA868C treatment group. The combining capacity of CRTH2 and DP total combining capacity on EOS in asthma group, BAYu3405 treatment group and BWA868C treatment group were significantly higher than those in Group A (P<0.01). There was no significant difference in DP1 among all the groups (P>0.05).
  
  
  
  CRTH2, but not DP1 antagonist can effectively ameliorate airway inflammation in rats with asthma.
authors.affiliation: Central Laboratory of Molecular Biology, Jinhua College of Profession and Technology, Jinhua, China.
authors.forename: Hong-qiang
authors.initials: HQ
authors.lastname: Lou
authors.forename: Yan-feng
authors.initials: YF
authors.lastname: Ying
authors.forename: Ye
authors.initials: Y
authors.lastname: Hu
mesh_terms: D000818:Animals; D001249:Asthma / Q000139:chemically induced / Q000188:drug therapy* / Q000473:pathology; D001980:Bronchi / Q000276:immunology / Q000473:pathology*; D002227:Carbazoles / Q000494:pharmacology / Q000627:therapeutic use*; D007249:Inflammation / Q000188:drug therapy*; D008297:Male; D010047:Ovalbumin; D015230:Prostaglandin D2 / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D011971:Receptors, Immunologic / Q000037:antagonists & inhibitors*; D011982:Receptors, Prostaglandin / Q000037:antagonists & inhibitors*; D013449:Sulfonamides / Q000494:pharmacology / Q000627:therapeutic use*
chemical_list: D002227:Carbazoles; D011971:Receptors, Immunologic; D011982:Receptors, Prostaglandin; D013449:Sulfonamides; D010047:Ovalbumin; C063119:ramatroban; D015230:Prostaglandin D2; C036293:prostaglandin D2 receptor