NADPH oxidase 2 does not contribute to early reperfusion-associated reactive oxygen species generation following transient focal cerebral ischemia
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Summary
The results suggest that Nox2 may not contribute to the early burst of reperfusions-related ROS generation, but is rather an important source of ROS generation during prolonged reperfusion.
- Type
- article
- Published
- 2016-11-01
- Cited by
- 10
- References
- 39
- Access
- Open access
- OpenAlex
- https://openalex.org/W2572633095
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:4975980
Keywords
NADPH oxidase, Reactive oxygen species, Ischemia, Western blot, Reperfusion injury
References
- Inhibition of the Rac1 GTPase protects against nonlethal ischemia/reperfusion‐induced necrosis and apoptosis in vivo
- NADPH oxidase mediates the expression of MMP-9 in cerebral tissue after ischemia–reperfusion damage
- Does normobaric hyperoxia increase oxidative stress in acute ischemic stroke? A critical review of the literature
- Interaction between NADPH‐oxidase and Rho‐kinase in angiotensin II‐induced microglial activation
- Translational Stroke Research of the Combination of Thrombolysis and Antioxidant Therapy
- Neuronal expression of the NADPH oxidase NOX4, and its regulation in mouse experimental brain ischemia.
- A review of oxygen therapy in ischemic stroke
- Matrix metalloproteinase-2-mediated occludin degradation and caveolin-1-mediated claudin-5 redistribution contribute to blood brain barrier damage in early ischemic stroke stage
- Human monocytes and macrophages express NADPH oxidase 5; a potential source of reactive oxygen species in atherosclerosis.
- Expression and Modulation of an NADPH Oxidase in Mammalian Astrocytes
- NADPH oxidase mediates the oxygen-glucose deprivation/reperfusion-induced increase in the tyrosine phosphorylation of the N-methyl-D-aspartate receptor NR2A subunit in retinoic acid differentiated SH-SY5Y Cells
- Xanthine oxidase is one of the major sources of superoxide anion radicals in blood after reperfusion in rats with forebrain ischemia/reperfusion.
- Which NADPH Oxidase Isoform Is Relevant for Ischemic Stroke? The Case for Nox 2
- Normobaric hyperoxia inhibits NADPH oxidase-mediated matrix metalloproteinase-9 induction in cerebral microvessels in experimental stroke
- Prodigiosin inhibits gp91(phox) and iNOS expression to protect mice against the oxidative/nitrosative brain injury induced by hypoxia-ischemia.
- Role of Neuronal NADPH Oxidase 1 in the Peri-Infarct Regions after Stroke
- Neuroprotection conferred by post‐ischemia ethanol therapy in experimental stroke: an inhibitory effect on hyperglycolysis and NADPH oxidase activation
- Neuronal NAD(P)H oxidases contribute to ROS production and mediate RGC death after ischemia.
- NOX family NADPH oxidases: not just in mammals.
- Nox2 Knockout Delays Infarct Progression and Increases Vascular Recovery through Angiogenesis in Mice following Ischaemic Stroke with Reperfusion
Cited by
- In vivo electron paramagnetic resonance oximetry and applications in the brain
- Dihydrocapsaicin Attenuates Blood Brain Barrier and Cerebral Damage in Focal Cerebral Ischemia/Reperfusion via Oxidative Stress and Inflammatory
- Using drugs to target necroptosis: dual roles in disease therapy.
- Mechanism of miR-320 in Regulating Biological Characteristics of Ischemic Cerebral Neuron by Mediating Nox2/ROS Pathway
- miR-124-5p/NOX2 Axis Modulates the ROS Production and the Inflammatory Microenvironment to Protect Against the Cerebral I/R Injury
- Knockout of Farnesoid X receptor Aggravates Process of Diabetic Cardiomyopathy.
- Acute administration of the olive constituent, oleuropein, combined with ischemic postconditioning increases myocardial protection by modulating oxidative defense.
- Role of Oxygen and Its Radicals in Peripheral Nerve Regeneration: From Hypoxia to Physoxia to Hyperoxia
- Cycloastragenol protected hippocampal CA1 neurons by regulating redox homeostasis and alleviated cognitive impairment following cerebral ischemia-reperfusion.
- NOX2/4 INHIBITION IN NB69 DURING ISCHEMIA/REPERFUSION
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