脳虚血へのグリア細胞のサイトカイン,ケモカイン,iNOS 誘導応答とニューロン死 The involvement of cytokines, chemokines and inducible nitric oxide synthase (iNOS) induced by a transient ischemia in neuronal survival/death in rat brain

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Inflammatory/immunological processes underlie the survival/damage of neurons after brain ischemia. In glial cells, cytokines such as IL-1β and TNF-α are produced following ischemic stresses. On the other hand, it is suggested that NO/iNOS is involved in neuronal apoptosis. We here review the ischemia-induced production of cytokine/iNOS and the neurotrophic/neurotoxic effects. It is not clear whether or not the neuronal death after brain ischemia is apoptosis or necrosis. Under the condition of transient forebrain ischemia, however, we obtained results suggesting apoptosis in the delayed neuronal death of the CA1 pyramidal neurons. The time course and cellular localization of postischemic iNOS expression depend on the properties of the ischemic insult. The iNOS induction is detected primarily in astrocytes after the transient forebrain ischemia when the neuronal apoptosis is observed. We discuss a variety of cytokines with neurotrophic/neurotoxic actions that are produced by ischemia or environmental stresses in glial cells. From the neurotoxicological aspect of the neuro-glial interaction, we also review recent findings on signaling pathways of the iNOS induction in glial cells and the mechanisms of the cytotoxic actions of NO.

収録刊行物

  • 日本薬理学雑誌

    日本薬理学雑誌 111(1), 37-44, 1998-01-01

    公益社団法人 日本薬理学会

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各種コード

  • NII論文ID(NAID)
    10008182021
  • NII書誌ID(NCID)
    AN00198335
  • 本文言語コード
    JPN
  • 資料種別
    REV
  • ISSN
    00155691
  • NDL 記事登録ID
    4382496
  • NDL 雑誌分類
    ZS51(科学技術--薬学)
  • NDL 請求記号
    Z19-247
  • データ提供元
    CJP書誌  NDL  J-STAGE 
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