酸化ストレスに対して神経細胞保護作用を有する化合物の作用機序の解明

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  • 原 宏和
    岐阜薬科大学医療薬剤学大講座臨床薬剤学研究室

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タイトル別名
  • Molecular Mechanism of Neuroprotective Drugs against Oxidative Stress-Induced Neuronal Cell Death
  • サンカ ストレス ニ タイシテ シンケイ サイボウ ホゴ サヨウ オ ユウスル カゴウブツ ノ サヨウ キジョ ノ カイメイ

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  NF-E2-related factor-2 (Nrf2), a basic leucine zipper transcription factor, is involved in the expression of numerous detoxifying and antioxidant genes via the antioxidant response element (ARE). Keap1, a cytoplasmic protein, sequesters Nrf2 in the cytoplasm under normal conditions. Various stimuli, including electrophiles and oxidative stress, liberate Nrf2 from Keap1, allowing Nrf2 to translocate into the nucleus and to bind to the ARE. Recently, there is increasing evidence that compounds that stimulate the activation of the Nrf2-ARE pathway may become useful therapeutic drugs for neurodegenerative diseases associated with oxidative stress. Apomorphine (Apo), a dopamine D1/D2 receptor agonist, is used for clinical therapy of Parkinson's disease. On the other hand, Apo is a potent radical scavenger and has protective effects on oxidative stress-induced cell death. We previously reported that pretreatment of human neuroblastoma SH-SY5Y cells with Apo enhanced the protective effects. In addition, we have recently demonstrated that Apo stimulates the translocation of Nrf2 into the nucleus and the transactivation of the ARE. Our findings suggest that not only the function as a radical scavenger, but also the function as an Nrf2-ARE pathway activator may be involved in the neuroprotective effects of Apo on oxidative stress-induced neuronal cell death. In this review, our recent studies on the mechanism underlying Apo-induced neuroprotection are summarized.<br>

収録刊行物

  • 薬学雑誌

    薬学雑誌 127 (8), 1199-1205, 2007-08-01

    公益社団法人 日本薬学会

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