The British journal of dermatology · 2007
Cyclooxygenase-1 inhibition delays recovery of the cutaneous barrier disruption caused by mechanical scratching in mice.
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Honma Y, Arai I, Futaki N, Hashimoto Y, Sugimoto M, Sakurai T, Nakaike S
Аннотация
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.
OBJECTIVES: 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.
OBJECTIVES: 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.