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PNAS:有助保护心脏的自由基

来源:新华网 2010-10-12 09:43

英国一项最新研究发现,与过去笼统认为自由基全都有害健康不同,实际上某些自由基可以帮助保护心脏健康。这将使人们重新思考现在一些为保护健康而全面清除自由基的疗法。

自由基是一类具有较强氧化性的原子或原子团的总称,它们常会损害正常的细胞和组织,因此现在许多疗法都试图使用抗氧化剂来全面去除自由基,以帮助保护健康。

但英国伦敦国王学院等机构研究人员在新一期美国《国家科学院学报》上报告说,动物实验显示一种名为Nox4的酶所生成的活性氧自由基有助保护心脏。研究人员改变了实验鼠的基因,使一些实验鼠体内有过多的这种酶而另一些实验鼠体内缺少这种酶。结果发现,在心脏面临高血压等压力的情况下,前一类实验鼠的心脏表现得更好。

参与研究的阿杰伊·沙阿教授说,自由基有一个“有害健康”的坏名声,因此许多疗法都试图全面清除它们,但很少有通过这种方式成功改善健康的例子。这项研究表明,某些自由基可以帮助心脏适应压力,对健康具有益处,因此相关疗法需要考虑区别对待不同的自由基,才能更有效地保护健康。(生物谷Bioon.com)

更多阅读

PNAS:羟基自由基产生分子机理新突破
FRBM:发现强自由基清除能力的抗氧化肽
Science:清除自由基 健康又长寿
Cell:羟基自由基-抗生素共有的“终极武器”
Nature:自由基可能与食欲调控有关
浙大成立自由基生命科学研究中心
衰老研究的新纪元
日本开发出用芝麻成分检测自由基的方法

生物谷推荐英文摘要:

PNAS doi: 10.1073/pnas.1002178107

NADPH oxidase 4 (Nox4) is a major source of oxidative stress in the failing heart
Junya Kurodaa, Tetsuro Agoa, Shouji Matsushimaa, Peiyong Zhaia, Michael D. Schneiderb, and Junichi Sadoshimaa,1

NAD(P)H oxidases (Noxs) produce O2? and play an important role in cardiovascular pathophysiology. The Nox4 isoform is expressed primarily in the mitochondria in cardiac myocytes. To elucidate the function of endogenous Nox4 in the heart, we generated cardiac-specific Nox4?/? (c-Nox4?/?) mice. Nox4 expression was inhibited in c-Nox4?/? mice in a heart-specific manner, and there was no compensatory up-regulation in other Nox enzymes. These mice exhibited reduced levels of O2? in the heart, indicating that Nox4 is a significant source of O2? in cardiac myocytes. The baseline cardiac phenotype was normal in young c-Nox4?/? mice. In response to pressure overload (PO), however, increases in Nox4 expression and O2? production in mitochondria were abolished in c-Nox4?/? mice, and c-Nox4?/? mice exhibited significantly attenuated cardiac hypertrophy, interstitial fibrosis and apoptosis, and better cardiac function compared with WT mice. Mitochondrial swelling, cytochrome c release, and decreases in both mitochondrial DNA and aconitase activity in response to PO were attenuated in c-Nox4?/? mice. On the other hand, overexpression of Nox4 in mouse hearts exacerbated cardiac dysfunction, fibrosis, and apoptosis in response to PO. These results suggest that Nox4 in cardiac myocytes is a major source of mitochondrial oxidative stress, thereby mediating mitochondrial and cardiac dysfunction during PO.

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