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核因子-B激活有助于通过氧化应激在超重/肥胖中年和老年人血管内皮功能障碍
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
概括
核因子-kappaB (NF-kappaB) 的活性有助于血管内皮功能障碍在老化和肥胖的人. 用盐酸抑制NF-kappaB改善了血管功能和减少了氧化应激,这表明它在这种功能障碍中起着关键作用.
科学领域:
- 心血管科学 心血管科学
- 分子生物学分子生物学
- 衰老研究研究 衰老研究
背景情况:
- 血管内皮功能障碍与衰老和肥胖有关.
- 核因子-kappaB (NF-kappaB) 活性是这种功能障碍的潜在贡献者.
研究的目的:
- 研究NF-kappaB在与年龄和肥胖相关的血管内皮功能障碍中的作用.
- 为了确定是否用盐酸抑制NF-kappaB可以改善老年人,超重/肥胖成人的内皮功能.
主要方法:
- 随机,双盲,安慰剂控制的交叉研究.
- 14 没有糖尿病,超重/肥胖,中年到老年人 (52-68岁).
- 在4天的时间内服用盐酸 (4500 mg/d) 或安慰剂.
主要成果:
- 盐酸治疗达到治疗性血度,并抑制内皮细胞中的NF-kappaB活性.
- 盐酸盐显著改善了流媒体扩张 (74%的增加),但不是内皮独立扩张.
- 盐酸盐在内皮细胞中降低了氧化应激的标志物 (尼托铁,NADPH氧化酶p47(phox)).
结论:
- 在超重和肥胖的老年人中,NF-kappaB在调解血管内皮功能障碍方面发挥着重要作用.
- 抑制NF-kappaB,部分通过减少氧化应激,改善内皮功能.
- 提供了NF-kappaB参与与年龄和肥胖相关的血管功能障碍的直接证据.
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