NADPH oxidase Nox1 contributes to ischemic injury in experimental stroke in mice
NADPH oxidase Nox1 contributes to ischemic injury in experimental stroke in mice
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DOI：
10.1016/j.nbd.2010.05.023
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发表时间：
2010-10-01
影响因子：
6.1
通讯作者：
Brandes, Ralf P.
中科院分区：
文献类型：
--
作者：
Kahles, Timo;Kohnen, Andreas;Brandes, Ralf P.
活性氧（reactive oxygen species，ROS）是脑缺血/再灌注损伤的介质。NADPH氧化酶Nox 2的参与已被证明。相比之下，只有很少有人知道的贡献，在这种情况下的Nox 1同源。因此，我们研究了Nox 1在大脑中动脉细丝闭塞模型中的早期脑再灌注损伤中的作用，使用Nox 1敲除小鼠。功能性Nox 1基因缺失导致缺血1小时后24小时病变大小减少55%（p
Reactive oxygen species (ROS) are mediators of brain injury in ischemia/reperfusion. An involvement of the NADPH oxidase Nox2 has been demonstrated. In contrast, only little is known about the contribution of the Nox1 homologue in this context. Thus, we studied the role of Nox1 in early cerebral reperfusion injury in the middle cerebral artery filament occlusion model using Nox1 knockout mice. Genetic deletion of a functional Nox1 lead to a 55% attenuation in lesion size at 24 h after induction of 1 h ischemia (p