期刊论文详细信息
International Journal of Molecular Sciences
NADPH Oxidase-Related Pathophysiology in Experimental Models of Stroke
Toru Nabika1  Tetsuro Ago2  Takanari Kitazono2  Hiroshi Yao3 
[1] Department of Functional Pathology, Shimane University School of Medicine, Izumo 693-8501, Japan;Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan;Laboratory of Neurochemistry, National Hospital Organization Hizen Psychiatric Center, Saga 842-0192, Japan;
关键词: stroke;    reactive oxygen species;    focal ischemia;    spontaneously hypertensive rats;    pericytes;    blood-brain barrier;    ischemic penumbra;   
DOI  :  10.3390/ijms18102123
来源: DOAJ
【 摘 要 】

Several experimental studies have indicated that nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (Nox) exert detrimental effects on ischemic brain tissue; Nox-knockout mice generally exhibit resistance to damage due to experimental stroke following middle cerebral artery occlusion (MCAO). Furthermore, our previous MCAO study indicated that infarct size and blood-brain barrier breakdown are enhanced in mice with pericyte-specific overexpression of Nox4, relative to levels observed in controls. However, it remains unclear whether Nox affects the stroke outcome directly by increasing oxidative stress at the site of ischemia, or indirectly by modifying physiological variables such as blood pressure or cerebral blood flow (CBF). Because of technical problems in the measurement of physiological variables and CBF, it is often difficult to address this issue in mouse models due to their small body size; in our previous study, we examined the effects of Nox activity on focal ischemic injury in a novel congenic rat strain: stroke-prone spontaneously hypertensive rats with loss-of-function in Nox. In this review, we summarize the current literature regarding the role of Nox in focal ischemic injury and discuss critical issues that should be considered when investigating Nox-related pathophysiology in animal models of stroke.

【 授权许可】

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