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Int J Mol Sci. 2017 Oct 11;18(10). pii: E2123. doi: 10.3390/ijms18102123.

NADPH Oxidase-Related Pathophysiology in Experimental Models of Stroke.

Author information

1
Laboratory of Neurochemistry, National Hospital Organization Hizen Psychiatric Center, Saga 842-0192, Japan. rinkenyao@abelia.ocn.ne.jp.
2
Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan. agou@intmed2.med.kyushu-u.ac.jp.
3
Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan. kitazono@intmed2.med.kyushu-u.ac.jp.
4
Department of Functional Pathology, Shimane University School of Medicine, Izumo 693-8501, Japan. nabika@med.shimane-u.ac.jp.

Abstract

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.

KEYWORDS:

blood-brain barrier; focal ischemia; ischemic penumbra; pericytes; reactive oxygen species; spontaneously hypertensive rats; stroke

PMID:
29019942
PMCID:
PMC5666805
DOI:
10.3390/ijms18102123
[Indexed for MEDLINE]
Free PMC Article

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