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核因子Bの活性化は,過体重/肥満中年および高齢のヒトにおける酸化ストレスによる血管内皮機能障害に寄与する
Gary L Pierce1, Lisa A Lesniewski, Brooke R Lawson
1Department of Integrative Physiology, University of Colorado at Boulder, 80309, USA. gpierce@colorado.edu
Circulation
|February 25, 2009
まとめ
核因子-kappaB (NF-kappaB) の活動は,老化および肥満のヒトにおける血管内皮機能不全に寄与する. 塩酸でNF-kappaBを阻害すると,血管機能が改善され,酸化ストレスが軽減され,この機能障害における重要な役割が示唆されています.
科学分野:
- 心血管科学 心血管科学
- 分子生物学は分子生物学である.
- 老化に関する研究
背景:
- 血管内皮機能不全は,老化と肥満に関連しています.
- 核因子-kappaB (NF-kappaB) の活動は,この機能不全の潜在的要因である.
研究 の 目的:
- 年齢および肥満に関連する血管内皮機能不全におけるNF-kappaBの役割を調査する.
- 塩酸でNF-kappaBを阻害することで,高齢者,肥満者,肥満者の内皮機能を改善できるかどうかを判断する.
主な方法:
- ランダム化,ダブルブラインド,プラセボ対照クロスオーバー研究.
- 14 糖尿病でない者,肥満者,中年から高齢者 (52-68歳).
- サルサラート (4500 mg/d) またはプラセボを4日間投与する.
主要な成果:
- サルサラート治療は,治療用プラズマ濃度に達し,内皮細胞におけるNF-kappaBの活性を抑制しました.
- サルサラートは,フローメディエーションによる膨張 (74%増加) を有意に改善したが,内皮独立の膨張は改善しなかった.
- サルサラートは,内皮細胞における酸化ストレスマーカー (ニトロチロシン,NADPH酸化酵素p47 (((phox)) を減少させた.
結論:
- NF-kappaBは,過体重および肥満の高齢者の血管内皮機能不全を媒介する重要な役割を果たします.
- NF-kappaBの抑制は,部分的に酸化的ストレスを軽減することによって,内皮機能を改善します.
- NF-kappaBが年齢および肥満に関連する血管機能障害に関与する直接的な証拠を提供します.
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