アデノシンA(1) 受容体の活性化により,マングネス超酸化物ディスミュータゼによって媒介されたラットにおける遅延した予備条件付けが誘発されます
A Dana1, A K Jonassen, N Yamashita
1Hatter Institute and Centre for Cardiology, University College London Hospitals and Medical School, London, UK.
Circulation
|June 22, 2000
まとめ
アデノシンA(1) 受容体の活性化により,ネズミの心臓保護が遅れている. この保護は,抗酸化酵素であるミトコンドリアマングネス超酸化物ディスミュータゼ (Mn-SOD) の増加によって媒介されます.
科学分野:
- 心血管研究 循環器科の研究
- ミトコンドリア生物学
- 薬理学 薬理学とは
背景:
- アデノシンA ((1) 受容体の活性化後にウサギで観察された遅れた心血管保護.
- この保護を媒介するミトコンドリアのマンガン超酸化物ディスミュータゼ (Mn-SOD) の役割を調査した.
研究 の 目的:
- アデノシンA(1) 受容体 (A(1) R) の活性化がラットにおける遅延した心臓保護を誘発するかどうかを判断する.
- この保護効果におけるミトコンドリアMn-SODの役割を明らかにする.
主な方法:
- ネズミは,A(1) RアゴニストであるCCPAまたは塩水,Mn-SODアンチセンセスのオリゴデオキシヌクレオチド (ODN) を含んでいるか否かを投与された.
- 心臓は,治療後24時間以内に地域性缺血と再注血を受けた.
- 心臓発作の大きさ,心筋のMn-SOD含有量,および活動が評価されました.
主要な成果:
- CCPAは,対照群と比較して心臓発作のサイズを大幅に減少させた (22.3%対42.1%).
- Antisense ODNはCCPA誘発の心臓保護を廃止しました.
- CCPAは,心筋のMn-SODの含有量と活動を増加させ,反感覚ODNによってブロックされた効果でした.
結論:
- 暫定的なA(1)R活性化により,ネズミの心臓保護が遅れる.
- ミトコンドリアのMn-SODは,この遅延保護におけるエンドエフェクターとして重要な役割を果たします.
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