ArticleFree radical biology & medicine2014
A time course of NADPH-oxidase up-regulation and endothelial nitric oxide synthase activation in the hippocampus following neurotrauma.
Article in Free radical biology & medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 40 citations in OpenAlex.
- Nitric oxide and traumatic brain injury.Medical gas research · 2027Review
- Mitochondrial-targeted therapies in traumatic brain injury: From bench to bedside.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
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- Biochemical regulatory processes in the control of oxidants and antioxidants production in the brain of rats with iron and copper chronic overloads.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2022Article
- Pharmacological Effects ofPharmaceuticals (Basel, Switzerland) · 2022Article
- Nitric oxide, chronic iron and copper overloads and regulation of redox homeostasis in rat liver.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2022Article
- The Role of NADPH Oxidase in Neuronal Death and Neurogenesis after Acute Neurological Disorders.Antioxidants (Basel, Switzerland) · 2021Review
- Estrogen and Bisphenol A in Hypertension.Current hypertension reports · 2020Review
- The Antitumor Efficacy ofBioMed research international · 2020Review
- Exposure to mild blast forces induces neuropathological effects, neurophysiological deficits and biochemical changes.Molecular brain · 2018Article
- NADPH oxidases in traumatic brain injury - Promising therapeutic targets?Redox biology · 2018Review
- White matter damage after traumatic brain injury: A role for damage associated molecular patterns.Biochimica et biophysica acta. Molecular basis of disease · 2017Review
- Natural Compounds as a Therapeutic Intervention following Traumatic Brain Injury: The Role of Phytochemicals.Journal of neurotrauma · 2017Review
- Central Nervous System Injury and Nicotinamide Adenine Dinucleotide Phosphate Oxidase: Oxidative Stress and Therapeutic Targets.Journal of neurotrauma · 2017Review
- Activation of p47phox as a Mechanism of Bupivacaine-Induced Burst Production of Reactive Oxygen Species and Neural Toxicity.Oxidative medicine and cellular longevity · 2017Article
- Salubrinal reduces oxidative stress, neuroinflammation and impulsive-like behavior in a rodent model of traumatic brain injury.Brain research · 2016Article
- Vitamins and nutrients as primary treatments in experimental brain injury: Clinical implications for nutraceutical therapies.Brain research · 2016Review
- Pycnogenol protects CA3-CA1 synaptic function in a rat model of traumatic brain injury.Experimental neurology · 2016Article
- Activation of Cannabinoid Receptor 2 Ameliorates DSS-Induced Colitis through Inhibiting NLRP3 Inflammasome in Macrophages.PloS one · 2016Article
- Acupuncture elicits neuroprotective effect by inhibiting NAPDH oxidase-mediated reactive oxygen species production in cerebral ischaemia.Scientific reports · 2015Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Nicotinamide adenine dinucleotide phosphate oxidase (NADPH-oxidase; NOX) is a complex enzyme responsible for increased levels of reactive oxygen species (ROS), superoxide (O2(•-)). NOX-derived O2(•-) is a key player in oxidative stress and inflammation-mediated multiple secondary injury cascades (SIC) following traumatic brain injury (TBI). The O2(•-) reacts with nitric oxide (NO), produces various reactive nitrogen species (RNS), and contributes to apoptotic cell death. Following a unilateral cortical contusion, young adult rats were killed at various times postinjury (1, 3, 6, 12, 24, 48, 72, and 96 h). Fresh tissue from the hippocampus was analyzed for NOX activity, and level of O2(•-). In addition we evaluated the translocation of cytosolic NOX proteins (p67(Phox), p47(Phox), and p40(Phox)) to the membrane, along with total NO and the activation (phosphorylation) of endothelial nitric oxide synthase (p-eNOS). Results show that both enzymes and levels of O2(•-) and NO have time-dependent injury effects in the hippocampus. Translocation of cytosolic NOX proteins into membrane, NOX activity, and O2(•-) were also increased in a time-dependent fashion. Both NOX activity and O2(•-) were increased at 6 h. Levels of p-eNOS increased within 1h, with significant elevation of NO at 12h post-TBI. Levels of NO failed to show a significant association with p-eNOS, but did associate with O2(•-). NOX up-regulation strongly associated with both the levels of O2(•-) and the total NO. The initial 12 h post-TBI are very important as a possible window of opportunity to interrupt SIC. It may be important to selectively target the translocation of cytosolic subunits for the modulation of NOX function.
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