Prostaglandin D2 and prostaglandin E2 accelerate the recovery of cutaneous barrier disruption induced by mechanical scratching in mice.
The role of prostaglandins in mechanical scratching-induced cutaneous barrier disruption in mice was investigated. Skin prostaglandins contents were measured after cutaneous barrier function was disrupted by scratching using a stainless-steal wire brush (mechanical scratching), then effects of prostanoids on recovery of cutaneous barrier functions were examined. This mechanical scratching increased transepidermal water loss and skin prostaglandins (prostaglandin D2, prostaglandin E2, 6-keto-prostaglandin F1alpha and prostaglandin F2alpha) contents, count-dependently. Topical application of indomethacin immediately after cutaneous barrier disruption delayed the recovery period of cutaneous barrier disruption. We examined effects of several prostanoids (prostaglandin D2, prostaglandin E2, prostaglandin F2alpha, prostaglandin I2 and U46619) on delay of the recovery process of mechanical scratching-induced cutaneous barrier disruption with treatment of indomethacin. Topically applied prostaglandin D2 and prostaglandin E2 accelerated the recovery of cutaneous barrier disruption and topical application of prostaglandin J2, limaprost, sulprostone and ONO-4819, but not 13,14-dihydro-15-keto-prostaglandin D2, 15-deoxy-Delta(12,14)-prostaglandin J2, 17-phenyl-trinor-prostaglandin E2 or butaprost had effects on recovery of the cutaneous barrier. These results suggest that prostaglandin D2 and prostaglandin E2 accelerate the recovery process of cutaneous barrier disruption caused by mechanical scratching, via specific prostanoid DP1, EP3 and EP4 receptors.
Department of Pharmacology Laboratory, Medical Research Laboratories, Taisho Pharmaceutical Co. Ltd., 1-403, Saitama City, Saitama 331-9530, Japan. y.honma@po.rd.taisho.co.jp
Yusuke
Y
Honma
Iwao
I
Arai
Yuki
Y
Hashimoto
Nobuko
N
Futaki
Masanori
M
Sugimoto
Makoto
M
Tanaka
Shiro
S
Nakaike
D015121:6-Ketoprostaglandin F1 alpha / Q000032:analysis; D000527:Alprostadil / Q000031:analogs & derivatives / Q000494:pharmacology; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D015237:Dinoprost / Q000032:analysis; D015232:Dinoprostone / Q000031:analogs & derivatives / Q000032:analysis / Q000494:pharmacology / Q000502:physiology*; D004305:Dose-Response Relationship, Drug; D006537:Heptanoates / Q000494:pharmacology; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D015230:Prostaglandin D2 / Q000031:analogs & derivatives / Q000032:analysis / Q000494:pharmacology / Q000502:physiology*; D011537:Pruritus / Q000503:physiopathology*; D018078:Receptors, Prostaglandin E / Q000819:agonists; D058309:Receptors, Prostaglandin E, EP4 Subtype; D012867:Skin / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology*; D013314:Stress, Mechanical; D013997:Time Factors; D014870:Water Loss, Insensible / Q000187:drug effects / Q000502:physiology
D000894:Anti-Inflammatory Agents, Non-Steroidal; D006537:Heptanoates; C487764:ONO4819; C545651:Ptger4 protein, mouse; D018078:Receptors, Prostaglandin E; D058309:Receptors, Prostaglandin E, EP4 Subtype; C016767:sulprostone; D015121:6-Ketoprostaglandin F1 alpha; C037112:9-deoxy-delta-9-prostaglandin D2; D015237:Dinoprost; D000527:Alprostadil; D015232:Dinoprostone; C059238:limaprost; D015230:Prostaglandin D2; D007213:Indomethacin