Abstract
Stroke is a leading cause of death and disability in humans. The excessive production of reactive oxygen species (ROS) is an important contributor to oxidative stress and secondary brain damage after stroke. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, an enzyme complex consisting of membrane subunits and cytoplasmic subunits, regulates neuronal maturation and cerebrovascular homeostasis. However, NADPH oxidase overproduction contributes to neurotoxicity and cerebrovascular disease. NADPH oxidase has been implicated as the principal source of ROS in the brain, and numerous studies have shown that the knockout of NADPH exerts a protective effect in the model of ischemic stroke. In this review, we summarize the mechanism of activation of the NADPH oxidase family members, the pathophysiological effects of NADPH oxidase isoforms in ischemic stroke, and the studies of NADPH oxidase inhibitors to explore potential clinical applications.
Highlights
Ischemic stroke is by far the most common type of stroke [1] and poses a significant global burden on healthcare
A study found that salivary GSH has high sensitivity and specificity differentiates different stages of dementia severity, and additional studies demonstrated that high serum levels of MDA and 8-OHdG are associated with early cognitive impairment after stroke; these redox biomarkers may be used as noninvasive biomarkers of cognitive impairment in the future [2, 12, 13]
Regarding the central nervous system, Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-derived reactive oxygen species (ROS) are necessary for normal brain function, including neuronal differentiation and neuronal signaling, but overproduction of ROS contributes to nervous system disease
Summary
Ischemic stroke is by far the most common type of stroke [1] and poses a significant global burden on healthcare. Research has demonstrated that oxidative stress is closely related to ischemic stroke sequelae. The excessive generation of ROS is thought to arise from a series of reasons including mitochondrial electron transport chain (ETC) dysfunction, induction of cyclooxygenases (COXs), increased expression of NADPH oxidase, N-methyl-D-aspartate (NMDA) receptor stimulation, and ceramide elevation after stroke [6,7,8]. A study found that salivary GSH has high sensitivity and specificity differentiates different stages of dementia severity, and additional studies demonstrated that high serum levels of MDA and 8-OHdG are associated with early cognitive impairment after stroke; these redox biomarkers may be used as noninvasive biomarkers of cognitive impairment in the future [2, 12, 13]. Researchers indicated that the ROS level was increased in the brain tissue after stroke onset, and NOX inhibitors exert a neuroprotective effect [27, 28]
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