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Prostanoid DP1 receptor agonist inhibits the pruritic activity in NC/Nga mice with atopic dermatitis.
Eur J Pharmacol. 2004 Nov 28; 505(1-3):229-35.EJ

Abstract

NC/Nga mice have similar pathological and behavioral features of human atopic dermatitis and are used as a model of the disease. Under conventional circumstances, spontaneous and persistent scratching is frequent and can lead to the onset of skin inflammation. We examined the effects of several prostanoids and their related compounds on the scratching behavior of NC/Nga mice. Among them, topically applied prostaglandin D2, prostaglandin E1, prostaglandin E2 and prostaglandin I2 significantly suppressed the scratching, the order of inhibitory activities being prostaglandin D2>>prostaglandin I2>prostaglandin E1=prostaglandin E2. Prostaglandin D2 metabolite, prostaglandin J2 also significantly suppressed the scratching but not so 13,14-dihydro-15-keto-prostaglandin D2, and 15-deoxy-Delta12,14-prostaglandin J2. The order of the inhibitory activities of these prostaglandin D2 metabolites depended on affinity of the prostanoid DP1 receptor but not on the DP2 receptor (chemoattractant receptor-homologous molecule expressed on T helper2 cells, CRTH2) and PPAR-gamma receptors. Likewise, topically applied arachidonic acid significantly suppressed the scratching while indomethacin enhanced it. Pretreatment of arachidonic acid increased the skin prostaglandins (prostaglandin D2, prostaglandin E2, prostaglandin F2alpha and 6-keto-prostaglandin F1alpha) contents, but indomethacin decreased the prostaglandin D2 and prostaglandin E2 contents. On the other hand, prostaglandin D2 and indomethacin had no apparent effects on histamine-induced scratching of ICR mice. These results suggested that prostaglandin D2 plays a physiological role in inhibiting pruritus of NC/Nga mice via their specific prostanoid DP1 receptors, and that prostaglandin D2 and/or a prostanoid DP1 receptor agonist may have therapeutic effects for cases of consecutive skin inflammation.

Authors+Show Affiliations

Department of Pharmacology, Medicinal Research Laboratories, Taisho Pharmaceutical Co., Ltd., 1-403 Yoshino-cho, Kita-ku, Saitama 331-9530, Japan. i.arai@po.rd.taisho.co.jpNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article

Language

eng

PubMed ID

15556157

Citation

Arai, Iwao, et al. "Prostanoid DP1 Receptor Agonist Inhibits the Pruritic Activity in NC/Nga Mice With Atopic Dermatitis." European Journal of Pharmacology, vol. 505, no. 1-3, 2004, pp. 229-35.
Arai I, Takano N, Hashimoto Y, et al. Prostanoid DP1 receptor agonist inhibits the pruritic activity in NC/Nga mice with atopic dermatitis. Eur J Pharmacol. 2004;505(1-3):229-35.
Arai, I., Takano, N., Hashimoto, Y., Futaki, N., Sugimoto, M., Takahashi, N., Inoue, T., & Nakaike, S. (2004). Prostanoid DP1 receptor agonist inhibits the pruritic activity in NC/Nga mice with atopic dermatitis. European Journal of Pharmacology, 505(1-3), 229-35.
Arai I, et al. Prostanoid DP1 Receptor Agonist Inhibits the Pruritic Activity in NC/Nga Mice With Atopic Dermatitis. Eur J Pharmacol. 2004 Nov 28;505(1-3):229-35. PubMed PMID: 15556157.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Prostanoid DP1 receptor agonist inhibits the pruritic activity in NC/Nga mice with atopic dermatitis. AU - Arai,Iwao, AU - Takano,Norikazu, AU - Hashimoto,Yuki, AU - Futaki,Nobuko, AU - Sugimoto,Masanori, AU - Takahashi,Nobutaka, AU - Inoue,Tomoyuki, AU - Nakaike,Shiro, PY - 2004/10/05/received PY - 2004/10/12/accepted PY - 2004/11/24/pubmed PY - 2005/5/17/medline PY - 2004/11/24/entrez SP - 229 EP - 35 JF - European journal of pharmacology JO - Eur J Pharmacol VL - 505 IS - 1-3 N2 - NC/Nga mice have similar pathological and behavioral features of human atopic dermatitis and are used as a model of the disease. Under conventional circumstances, spontaneous and persistent scratching is frequent and can lead to the onset of skin inflammation. We examined the effects of several prostanoids and their related compounds on the scratching behavior of NC/Nga mice. Among them, topically applied prostaglandin D2, prostaglandin E1, prostaglandin E2 and prostaglandin I2 significantly suppressed the scratching, the order of inhibitory activities being prostaglandin D2>>prostaglandin I2>prostaglandin E1=prostaglandin E2. Prostaglandin D2 metabolite, prostaglandin J2 also significantly suppressed the scratching but not so 13,14-dihydro-15-keto-prostaglandin D2, and 15-deoxy-Delta12,14-prostaglandin J2. The order of the inhibitory activities of these prostaglandin D2 metabolites depended on affinity of the prostanoid DP1 receptor but not on the DP2 receptor (chemoattractant receptor-homologous molecule expressed on T helper2 cells, CRTH2) and PPAR-gamma receptors. Likewise, topically applied arachidonic acid significantly suppressed the scratching while indomethacin enhanced it. Pretreatment of arachidonic acid increased the skin prostaglandins (prostaglandin D2, prostaglandin E2, prostaglandin F2alpha and 6-keto-prostaglandin F1alpha) contents, but indomethacin decreased the prostaglandin D2 and prostaglandin E2 contents. On the other hand, prostaglandin D2 and indomethacin had no apparent effects on histamine-induced scratching of ICR mice. These results suggested that prostaglandin D2 plays a physiological role in inhibiting pruritus of NC/Nga mice via their specific prostanoid DP1 receptors, and that prostaglandin D2 and/or a prostanoid DP1 receptor agonist may have therapeutic effects for cases of consecutive skin inflammation. SN - 0014-2999 UR - https://www.unboundmedicine.com/medline/citation/15556157/Prostanoid_DP1_receptor_agonist_inhibits_the_pruritic_activity_in_NC/Nga_mice_with_atopic_dermatitis_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-2999(04)01201-4 DB - PRIME DP - Unbound Medicine ER -