アディポネクチンは,内皮の酸化窒素合成酵素に依存するメカニズムを通じて,脳不全性損傷を予防します
Masaki Nishimura1, Yasuhiro Izumiya, Akiko Higuchi
1Stroke and Neurovascular Regulation Laboratory, Boston University School of Medicine, Boston, MA, USA.
Circulation
|December 26, 2007
まとめ
アディポネクチン欠乏症は,マウスの脳卒中後の脳損傷を悪化させる. アディポネクチンを補充すると,窒素酸化物の生成を高めることで脳卒中の損傷を軽減し,それを示唆しています.
科学分野:
- 心血管研究 循環器科の研究
- 神経科学は神経科学である.
- エンドクリノロジー エンドクリノロジー
背景:
- 脂肪由来タンパク質であるアディポネクチンは,心血管の健康に有益です.
- 低アディポネクチンのレベルは,脳卒中後の高死亡率と相関しています.
- 缺血性脳卒中におけるアディポネクチンの直接的な役割は不明である.
研究 の 目的:
- 急性脳損傷におけるアディポネクチンの因果的役割を調査する.
- 発血性脳卒中に対するアディポネクチンの効果の基礎となるメカニズムを決定する.
主な方法:
- 中脳動脈閉塞 (MCAO) はアディポネクチン欠乏症 (APN-KO) と野生型 (WT) のマウスで.
- 脳梗塞と神経学的欠陥の評価.
- アデノウイルス媒介のアディポネクチンサプリメント.
- 脳の血流のためのレーザースペックルフローメトリ.
- タンパク質分析のための免疫ヒストキミストリーとウエスタン・ブロッティング.
主要な成果:
- APN-KOマウスは,WTマウスよりも大きな心臓発作と悪質な神経学的欠陥を示した.
- アディポネクチンサプリメントは,APN-KOとWTの両方のマウスで心臓発作のサイズを減少させた.
- APN-KOマウスは,脳の血流と酸化窒素 (NO) 産出が低下していた.
- アディポネクチンの投与は,内皮酸化窒素合成酵素 (eNOS) 経由でNOの産生を増加させた.
結論:
- アディポネクチンは,不全性脳卒中に対する脳保護を提供します.
- この保護効果は,内皮の酸化窒素合成酵素 (eNOS) 経路によって媒介されます.
- アディポネクチンは,不全性脳卒中を予防するための潜在的な治療目標です.
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