作者
Christina Doverhag, Matthias Keller, Anna Karlsson, Maj Hedtjarn, Ulf Nilsson, Edith Kapeller, Gergely Sarkozy, Lars Klimaschewski, Christian Humpel, Henrik Hagberg, Georg Simbruner, Pierre Gressens, Karin Savman
发表日期
2008/7/1
期刊
Neurobiology of disease
卷号
31
期号
1
页码范围
133-144
出版商
Academic Press
简介
BACKGROUND
Inflammation and reactive oxygen species (ROS) are important in the development of perinatal brain injury. The ROS-generating enzyme NADPH oxidase (Nox2) is present in inflammatory cells and contributes to brain injury in adult animal models.
HYPOTHESIS
NADPH oxidase contributes to ROS formation and development of injury in the immature brain and inhibition of NADPH oxidase attenuates perinatal brain injury.
METHODS
We used animal models of term hypoxia–ischemia (HI) (P9 mice) as well as ibotenate-induced excitotoxic injury (P5 mice) mimicking features of periventricular leukomalacia in preterm infants. In vitro microglia cell cultures were used to investigate NADPH oxidase-dependent ROS formation. In vivo we determined the impact 1) of HI on NADPH oxidase gene expression 2) of genetic (gp91-phox/Nox2 knock-out) and 3) of pharmacological NADPH oxidase inhibition on …
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C Doverhag, M Keller, A Karlsson, M Hedtjarn… - Neurobiology of disease, 2008