ArticleTranslational research : the journal of laboratory and clinical medicine2015
Amelioration of nicotinamide adenine dinucleotide phosphate-oxidase mediated stress reduces cell death after blast-induced traumatic brain injury.
Article in Translational research : the journal of laboratory and clinical medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 44 citations in OpenAlex.
- Exploring the Role of Alpha Lipoic Acid in the Treatment of Traumatic Brain Injury: Pathways and Perspectives.Neurocritical care · 2026Review
- Usefulness of Serum NOX4 as a Potential Biomarker to Predict Early Neurological Deterioration and Poor Outcome of Spontaneous Intracerebral Hemorrhage: A Prospective Observational Study.Neuropsychiatric disease and treatment · 2025Article
- Ginkgolide A attenuated apoptosis via inhibition of oxidative stress in mice with traumatic brain injury.Heliyon · 2024Article
- The Neurovascular Unit as a Locus of Injury in Low-Level Blast-Induced Neurotrauma.International journal of molecular sciences · 2024Review
- Neuroprotective Effects of Curcumin against Chronic Chlorpyrifos- Induced Oxidative Damage in Rat Brain Tissue.Current aging science · 2024Article
- Neuroprotective effects of mild hypothermia against traumatic brain injury by the involvement of the Nrf2/ARE pathway.Brain and behavior · 2022Article
- Modulation of astrocyte activity and improvement of oxidative stress through blockage of NO/NMDAR pathway improve posttraumatic stress disorder (PTSD)-like behavior induced by social isolation stress.Brain and behavior · 2022Article
- New insights into the interplay between autophagy and oxidative and endoplasmic reticulum stress in neuronal cell death and survival.Frontiers in cell and developmental biology · 2022Review
- Neuromodulatory roles ofAIMS neuroscience · 2022Article
- Brain and blood biomarkers of tauopathy and neuronal injury in humans and rats with neurobehavioral syndromes following blast exposure.Molecular psychiatry · 2021Article
- Progressive Cognitive and Post-Traumatic Stress Disorder-Related Behavioral Traits in Rats Exposed to Repetitive Low-Level Blast.Journal of neurotrauma · 2021Article
- Laterality and region-specific tau phosphorylation correlate with PTSD-related behavioral traits in rats exposed to repetitive low-level blast.Acta neuropathologica communications · 2021Article
- The NLRP3 inflammasome: a potential therapeutic target for traumatic brain injury.Neural regeneration research · 2021Article
- Multiple Mild Traumatic Brain Injuries Lead to Visual Dysfunction in a Mouse Model.Journal of neurotrauma · 2020Article
- Low-level blast exposure disrupts gliovascular and neurovascular connections and induces a chronic vascular pathology in rat brain.Acta neuropathologica communications · 2019Article
- A Single Primary Blast-Induced Traumatic Brain Injury in a Rodent Model Causes Cell-Type Dependent Increase in Nicotinamide Adenine Dinucleotide Phosphate Oxidase Isoforms in Vulnerable Brain Regions.Journal of neurotrauma · 2018Article
- NADPH oxidases in traumatic brain injury - Promising therapeutic targets?Redox biology · 2018Review
- Examining the Correlation between Acute Behavioral Manifestations of Concussion and the Underlying Pathophysiology of Chronic Traumatic Encephalopathy: A Pilot Study.Journal of neurology and psychology · 2018Article
- Supplements, nutrition, and alternative therapies for the treatment of traumatic brain injury.Nutritional neuroscience · 2018Review
- Wake-promoting effects of vagus nerve stimulation after traumatic brain injury: upregulation of orexin-A and orexin receptor type 1 expression in the prefrontal cortex.Neural regeneration research · 2018Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
A total of 1.7 million traumatic brain injuries (TBIs) occur each year in the United States, but available pharmacologic options for the treatment of acute neurotrauma are limited. Oxidative stress is an important secondary mechanism of injury that can lead to neuronal apoptosis and subsequent behavioral changes. Using a clinically relevant and validated rodent blast model, we investigated how nicotinamide adenine dinucleotide phosphate oxidase (Nox) expression and associated oxidative stress contribute to cellular apoptosis after single and repeat blast injuries. Nox4 forms a complex with p22phox after injury, forming free radicals at neuronal membranes. Using immunohistochemical-staining methods, we found a visible increase in Nox4 after single blast injury in Sprague Dawley rats. Interestingly, Nox4 was also increased in postmortem human samples obtained from athletes diagnosed with chronic traumatic encephalopathy. Nox4 activity correlated with an increase in superoxide formation. Alpha-lipoic acid, an oxidative stress inhibitor, prevented the development of superoxide acutely and increased antiapoptotic markers B-cell lymphoma 2 (t = 3.079, P < 0.05) and heme oxygenase 1 (t = 8.169, P < 0.001) after single blast. Subacutely, alpha-lipoic acid treatment reduced proapoptotic markers Bax (t = 4.483, P < 0.05), caspase 12 (t = 6.157, P < 0.001), and caspase 3 (t = 4.573, P < 0.01) after repetitive blast, and reduced tau hyperphosphorylation indicated by decreased CP-13 and paired helical filament staining. Alpha-lipoic acid ameliorated impulsive-like behavior 7 days after repetitive blast injury (t = 3.573, P < 0.05) compared with blast exposed animals without treatment. TBI can cause debilitating symptoms and psychiatric disorders. Oxidative stress is an ideal target for neuropharmacologic intervention, and alpha-lipoic acid warrants further investigation as a therapeutic for prevention of chronic neurodegeneration.
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Registered trials
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