Regulation of anti-inflammatory and anti-oxidative effects by liranaftate through aryl hydrocarbon receptor on human keratinocytes

Masakazu Takahara, Kenjiro Takei, Akiko Hachiya, Yukihiro Mizote, Mika Murai, Yoshiko Sasaki, Fumitaka Ohno, Noriko Okabe, Nobutoshi Take, Akiko Masuda, Masutaka Furue

研究成果: Contribution to journalArticle査読

抄録

The antimycotic drug liranaftate has been shown to have anti-inflammatory effects, but its mechanism of action is largely unknown. Many polycyclic aromatic hydrocarbons and other external chemicals bind to the cytosolic aryl hydrocarbon receptor (AhR), which is abundantly expressed in cultured human keratinocytes. Liranaftate induced nuclear translocation of AhR and nuclear factor-erythroid 2-related factor-2 (Nrf2) from the cytoplasm in the keratinocytes and upregulated mRNA for NAD(P)H : quinone oxidoreductase 1 (Nqo1) and Nrf2. TNFα-induced reactive oxidative species (ROS) and IL-8 production were effectively inhibited by liranaftate. Knockdown of AhR abolished liranaftate-induced Nqo1 and Nrf2 expressions as well as the inhibitory action on IL-8 production, suggesting an AhR-dependent mechanism of action. Additionally, liranaftate upregulated the mRNA expressions of skin barrier proteins such as filaggrin, loricrin and involucrin in an AhR-dependent fashion. These anti-inflammatory effects may partly explain the rapid and potent clinical efficacy against tinea by liranaftate.

本文言語英語
ページ(範囲)121-126
ページ数6
ジャーナルNishinihon Journal of Dermatology
76
2
DOI
出版ステータス出版済み - 2014

All Science Journal Classification (ASJC) codes

  • 皮膚病学

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