ラット中大脳動脈閉塞・再灌流後の iNOS の誘導と梗塞巣進展 Lack of evidence that inducible nitric oxide synthase participates in the development of ischemic brain damage

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We have already reported that the concentration of nitric oxide (NO) increases during and after cerebral ischemia and a selective inhibitor of neuronal NO synthase (nNOS) suppresses this increase and subsequently mitigates brain damage in rats. Although the selective inhibition of nNOS is a promising pharmacological strategy for the treatment of stroke, the role of inducible NOS (iNOS) remains to be clarified. Toward this end, we investigated temporal alterations in iNOS mRNA by the RT-PCR method in a rat model of middle cerebral artery (MCA) occlusion. We found that iNOS mRNA in the ischemic hemisphere began to increase at 3 hr and reached the maximum level at 24 hr of reperfusion following 3 hr of MCA occlusion. However, quantitative analysis revealed that no significant difference existed between 6 hr or 24 hr reperfusion group and their respective time-matched sham operation group. In addition, neither Western blotting nor immunocytochemical study disclosed an apparent induction of iNOS at any time points examined. Similar results were obtained at 24 hr of permanent MCA occlusion. Taken together, these data indicate that iNOS induction during and after MCA occlusion may be not a critical event for the development of infarction caused by ischemia itself.

収録刊行物

  • 日本薬理学雑誌

    日本薬理学雑誌 111(1), 45-53, 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)
    10008182065
  • 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
    4382497
  • 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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