脳虚血におけるバナジウム化合物の神経新生亢進作用

• 塩田 倫史

  東北大学大学院薬学研究科薬理学分野

• 森岡 基浩

  熊本大学医学部付属病院脳神経外科

• 福永 浩司

  東北大学大学院薬学研究科薬理学分野 東北大学21世紀COEプログラム“CRESCEND”

書誌事項

タイトル別名

• Vanadium Compounds Enhance Adult Neurogenesis after Brain Ischemia
• ノウキョケツ ニ オケル バナジウム カゴウブツ ノ シンケイ シンセイ コウシン サヨウ

抄録

  Generation of neural precursors persists throughout life in the forebrain subventricular zone (SVZ) and dentate gyrus (DG) subgranular zone (SGZ) in rodent and human brains. In addition, newborn granule cells in the hippocampal DG are important for learning and memory formation. Brain injuries such as seizures or trauma could trigger endogenous programs for adult neurogenesis. Although brain ischemia also increases proliferation of neural progenitor cells in SVZ and SGZ, most neural progenitor cells are dead within 2 weeks after brain ischemia. In addition, there is no therapeutic agent to promote neurogenesis in the adult brain following brain injury. Here we found that intraperitoneal administrations of vanadium compounds, a stimulator of phosphatidylinositol 3-kinase (PI3K)/Akt and extracellular signal regulated kinase (ERK) pathways markedly enhances brain ischemia-induced neurogenesis. Thus, vanadium compounds are potential therapeutic agent to enhance ischemia-induced neurogenesis through PI3K/Akt and ERK activation.<br>

収録刊行物

• 薬学雑誌

  薬学雑誌 128 (3), 413-417, 2008-03-01

  公益社団法人 日本薬学会

キーワード

• adult neurogenesis
• brain ischemia
• vanadium compound
• Akt
• extracellular signal regulated kinase (ERK)

詳細情報

• CRID: 1390282681104467968
• NII論文ID: 110006646595
• NII書誌ID: AN00284903
• DOI: 10.1248/yakushi.128.413
• ISSN: 13475231
• ISSN: 00316903
• NDL書誌ID: 9397426
• Web Site: http://id.ndl.go.jp/bib/9397426
• Web Site: https://ndlsearch.ndl.go.jp/books/R000000004-I9397426
• Web Site: https://www.jstage.jst.go.jp/article/yakushi/128/3/128_3_413/_pdf
• Web Site: https://search.jamas.or.jp/link/ui/2008175387
• 本文言語コード: ja
• データソース種別:
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  • NDL
  • Crossref
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• 抄録ライセンスフラグ: 使用不可