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Drug Development and Neuroprotection

開催日 2014/9/11
時間 9:00 - 10:00
会場 Room J(313+314)
Chairperson(s) 池田 華子 / Hanako Ohashi-Ikeda (京都大学医学部附属病院 臨床研究総合センター / Institute for Advancement of Clinical and Translational Science, Kyoto University Hospital, Japan)
東田 千尋 / Chihiro Tohda (富山大学和漢医薬学総合研究所神経機能学分野 / Division of Neuromedical Science, Institute of Natural Medicine, University of Toyama, Japan)

H2S-derived polysulfides are potential signaling molecules that activate TRPA1 channels in rat brain

  • O1-J-1-3
  • 木村 由佳 / Yuka Kimura:1 三上 義礼 / Yoshinori Mikami:2 大隅 貴美子 / Kimiko Osumi:1 津金 麻美子 / Mamiko Tsugane:3 岡 淳一郎 / Jun-ichiro Oka:4 
  • 1:国立精神・神経医療研究センター・神経研究所・神経薬理 / Dept Mol Pharmacol, National Inst Neuroscience, NCNP, Tokyo, Japan 2:東京大院・医・細胞分子薬理学 / Dept Pharmacol, Grad Sch Med, Univ of Tokyo, Tokyo, Japan 3:中央大・理工学部 / Fclty Sci Eng, Chuo Univ, Tokyo, Japan 4:東京理科大学・薬 / Dept Pharmacy, Tokyo Univ of Sci, Chiba, Japan 

Hydrogen sulfide (H2S) is emerging as bioactive substance with various physiological functions. H2S is enzymatically produced from cysteine by 3 kinds of sulfurtransferases, then is oxidized to polysulfides whose function is not well understood. We previously reported that polysulfides induce Ca2+ influx in astrocytes. However, the receptor that mediates the response has not been identified. Here, we have shown that polysulfides induce Ca2+ influx by activating transient receptor potential ankyrin-1 (TRPA1) channels in rat astrocytes. The maximum response is induced by 0.5 μM polysulfide, which is about 1/300 of the concentration of H2S required to achieve a response of similar magnitude. TRPA1-selective agonists, allyl isothiocyanate and cinnamaldehyde, induced Ca2+ influx, and responses to polysulfides were suppressed by TRPA1-selective inhibitors, HC-030031 and AP-18, as well as by siRNAs selective to TRPA1. The present study suggests that polysulfides are potential H2S-derived signaling molecules that stimulate TRPA1 channels in the brain.

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