title: Cyclooxygenase-1 inhibition delays recovery of the cutaneous barrier disruption caused by mechanical scratching in mice.
abstract: BACKGROUND
  Atopic dermatitis is a chronic inflammatory disease characterized by severe pruritus, and cutaneous barrier disruption by scratching contributes to further aggravation of the condition. We have previously shown that indomethacin delayed recovery from the effects of cutaneous barrier disruption caused by mechanical scratching in mice.
  
  
  OBJECTIVE
  This study was designed to assess the role of cyclooxygenase (COX)-1 and COX-2 inhibitors on recovery from the effects of cutaneous barrier disruption induced by mechanical scratching in mice.
  
  
  METHODS
  We examined the effects of SC-560 (a COX-1-selective inhibitor) or NS-398 (a COX-2-selective inhibitor) on recovery from the effects of cutaneous barrier disruption in mice induced by a wire brush, in terms of the skin prostaglandin (PG) levels.
  
  
  RESULTS
  While SC-560 significantly delayed recovery from the effects of cutaneous barrier disruption, NS-398 had no such effect. SC-560 was significantly more effective than NS-398 in reducing skin PG levels at 6 and 24 h after cutaneous barrier disruption. SC-560 strongly inhibited biosynthesis of cutaneous PGD(2) to a greater extent than that of other PGs.
  
  
  CONCLUSIONS
  COX-1-coupled PGD(2) biosynthesis may be an important factor in the recovery of cutaneous barrier disruption.
authors: Department of Pharmacology, Medicinal Research Laboratories, Taisho Pharmaceutical Co., Ltd, 1-403 Yoshino-cho, Kita-ku, Saitama 331-9530, Japan. y.honma@po.rd.taisho.co.jp
authors: Y
authors: Y
authors: Honma
authors: I
authors: I
authors: Arai
authors: N
authors: N
authors: Futaki
authors: Y
authors: Y
authors: Hashimoto
authors: M
authors: M
authors: Sugimoto
authors: T
authors: T
authors: Sakurai
authors: S
authors: S
authors: Nakaike
mesh_terms: D000818:Animals; D051545:Cyclooxygenase 1 / Q000032:analysis / Q000502:physiology*; D051546:Cyclooxygenase 2 / Q000032:analysis / Q000502:physiology*; D052246:Cyclooxygenase 2 Inhibitors / Q000494:pharmacology*; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology*; D003876:Dermatitis, Atopic / Q000378:metabolism*; D004487:Edema / Q000188:drug therapy; D007150:Immunohistochemistry; D007213:Indomethacin / Q000627:therapeutic use; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009578:Nitrobenzenes / Q000494:pharmacology; D010949:Plasma / Q000378:metabolism; D011453:Prostaglandins / Q000378:metabolism; D011537:Pruritus / Q000378:metabolism*; D011720:Pyrazoles / Q000494:pharmacology; D020127:Recovery of Function / Q000187:drug effects; D013449:Sulfonamides / Q000494:pharmacology
chemical_list: D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors; D009578:Nitrobenzenes; D011453:Prostaglandins; D011720:Pyrazoles; C115461:SC 560; D013449:Sulfonamides; C080955:N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; D007213:Indomethacin