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The anti-pruritic efficacy of TS-022, a prostanoid DP1 receptor agonist, is dependent on the endogenous prostaglandin D2 level in the skin of NC/Nga mice.
Eur J Pharmacol. 2007 Jun 14; 564(1-3):196-203.EJ

Abstract

TS-022 is a prostanoid DP(1) receptor agonist, originally developed as a novel anti-pruritic drug for atopic dermatitis. The drug has been shown to suppress scratching and improve the skin inflammation in the NC/Nga (NC) mouse, a model of atopic dermatitis. Corticosteroids are commonly used as effective agents for the treatment of atopic dermatitis. We examined the anti-pruritic efficacy of TS-022 in NC mice cohabited with skin-lesioned NC mice, which showed spontaneous scratching without skin lesions in the early phase and chronic itching with severe dermatitis in the late phase, in comparison with that of dexamethasone. We have previously reported that prostaglandin D(2) might have a physiological role in the inhibition of pruritus. While after 2 weeks of cohabitation with skin-lesioned NC mice (early phase of dermatitis, characterized by the appearance of spontaneous scratching), topically applied TS-022 exhibited a weak anti-pruritic effect in the NC mice, after 6 weeks of cohabitation (late phase, characterized by both chronic scratching and dermatitis), the drug exerted potent anti-pruritic activity. In contrast, dexamethasone exerted potent anti-pruritic effect in both the early and late phases. Indomethacin aggravated the scratching in the early phase, but had no effect in the late phase. The skin prostaglandin D(2) level was significantly increased in the early phase, to subsequently declined and return to the basal level in the late phase. The cutaneous ability for prostaglandin D(2) production following topical application of arachidonic acid or mechanical scratching was decreased in the late phase. Moreover, the expression level of the prostanoid DP(1) receptor in the skin was increased in the late phase. These findings suggest that the potent anti-pruritic activity of TS-022 in the late phase might be attributable to the decrease of endogenous prostaglandin D(2) production and increase of prostanoid DP(1) receptor expression.

Authors+Show Affiliations

Department of Pharmacology, Medicinal Research Laboratories, Taisho Pharmaceutical Co., Ltd., 1-403 Yoshino-cho, Kita-ku, Saitama 331-9530, Japan. masanori.sugimoto@po.rd.taisho.co.jpNo 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

17328887

Citation

Sugimoto, Masanori, et al. "The Anti-pruritic Efficacy of TS-022, a Prostanoid DP1 Receptor Agonist, Is Dependent On the Endogenous Prostaglandin D2 Level in the Skin of NC/Nga Mice." European Journal of Pharmacology, vol. 564, no. 1-3, 2007, pp. 196-203.
Sugimoto M, Arai I, Futaki N, et al. The anti-pruritic efficacy of TS-022, a prostanoid DP1 receptor agonist, is dependent on the endogenous prostaglandin D2 level in the skin of NC/Nga mice. Eur J Pharmacol. 2007;564(1-3):196-203.
Sugimoto, M., Arai, I., Futaki, N., Hashimoto, Y., Sakurai, T., Honma, Y., & Nakaike, S. (2007). The anti-pruritic efficacy of TS-022, a prostanoid DP1 receptor agonist, is dependent on the endogenous prostaglandin D2 level in the skin of NC/Nga mice. European Journal of Pharmacology, 564(1-3), 196-203.
Sugimoto M, et al. The Anti-pruritic Efficacy of TS-022, a Prostanoid DP1 Receptor Agonist, Is Dependent On the Endogenous Prostaglandin D2 Level in the Skin of NC/Nga Mice. Eur J Pharmacol. 2007 Jun 14;564(1-3):196-203. PubMed PMID: 17328887.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The anti-pruritic efficacy of TS-022, a prostanoid DP1 receptor agonist, is dependent on the endogenous prostaglandin D2 level in the skin of NC/Nga mice. AU - Sugimoto,Masanori, AU - Arai,Iwao, AU - Futaki,Nobuko, AU - Hashimoto,Yuki, AU - Sakurai,Takanobu, AU - Honma,Yusuke, AU - Nakaike,Shiro, Y1 - 2007/02/08/ PY - 2006/10/10/received PY - 2007/01/22/revised PY - 2007/01/24/accepted PY - 2007/3/3/pubmed PY - 2007/8/19/medline PY - 2007/3/3/entrez SP - 196 EP - 203 JF - European journal of pharmacology JO - Eur J Pharmacol VL - 564 IS - 1-3 N2 - TS-022 is a prostanoid DP(1) receptor agonist, originally developed as a novel anti-pruritic drug for atopic dermatitis. The drug has been shown to suppress scratching and improve the skin inflammation in the NC/Nga (NC) mouse, a model of atopic dermatitis. Corticosteroids are commonly used as effective agents for the treatment of atopic dermatitis. We examined the anti-pruritic efficacy of TS-022 in NC mice cohabited with skin-lesioned NC mice, which showed spontaneous scratching without skin lesions in the early phase and chronic itching with severe dermatitis in the late phase, in comparison with that of dexamethasone. We have previously reported that prostaglandin D(2) might have a physiological role in the inhibition of pruritus. While after 2 weeks of cohabitation with skin-lesioned NC mice (early phase of dermatitis, characterized by the appearance of spontaneous scratching), topically applied TS-022 exhibited a weak anti-pruritic effect in the NC mice, after 6 weeks of cohabitation (late phase, characterized by both chronic scratching and dermatitis), the drug exerted potent anti-pruritic activity. In contrast, dexamethasone exerted potent anti-pruritic effect in both the early and late phases. Indomethacin aggravated the scratching in the early phase, but had no effect in the late phase. The skin prostaglandin D(2) level was significantly increased in the early phase, to subsequently declined and return to the basal level in the late phase. The cutaneous ability for prostaglandin D(2) production following topical application of arachidonic acid or mechanical scratching was decreased in the late phase. Moreover, the expression level of the prostanoid DP(1) receptor in the skin was increased in the late phase. These findings suggest that the potent anti-pruritic activity of TS-022 in the late phase might be attributable to the decrease of endogenous prostaglandin D(2) production and increase of prostanoid DP(1) receptor expression. SN - 0014-2999 UR - https://www.unboundmedicine.com/medline/citation/17328887/The_anti_pruritic_efficacy_of_TS_022_a_prostanoid_DP1_receptor_agonist_is_dependent_on_the_endogenous_prostaglandin_D2_level_in_the_skin_of_NC/Nga_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-2999(07)00143-4 DB - PRIME DP - Unbound Medicine ER -