ArticleJournal of neurotrauma2014
Suppression of oxidative stress and 5-lipoxygenase activation by edaravone improves depressive-like behavior after concussion.
Article in Journal of neurotrauma, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Repeated impacts induce acute neurobehavioral and molecular deficits in a mouse model of traumatic brain injury.Experimental brain research · 2026Article
- Edaravone: Advances on cytoprotective effects, pharmacological properties, and mechanisms of action.Pharmacological reviews · 2026Review
- The role of arachidonic acid metabolites in major depressive disorder: mechanisms and therapeutic implications.Metabolic brain disease · 2025Review
- Traumatic brain injury and the development of parkinsonism: Understanding pathophysiology, animal models, and therapeutic targets.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022Review
- Edaravone attenuates neuronal apoptosis in hippocampus of rat traumatic brain injury model via activation of BDNF/TrkB signaling pathway.Archives of medical science : AMS · 2021Article
- Traumatic Brain Injury: Oxidative Stress and Novel Anti-Oxidants Such as Mitoquinone and Edaravone.Antioxidants (Basel, Switzerland) · 2020Review
- Edaravone attenuates traumatic brain injury through anti-inflammatory and anti-oxidative modulation.Experimental and therapeutic medicine · 2019Article
- Combined treatment with GSNO and CAPE accelerates functional recovery via additive antioxidant activities in a mouse model of TBI.Journal of neuroscience research · 2018Article
- A combination antioxidant therapy to inhibit NOX2 and activate Nrf2 decreases secondary brain damage and improves functional recovery after traumatic brain injury.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018Article
- Elucidating opportunities and pitfalls in the treatment of experimental traumatic brain injury to optimize and facilitate clinical translation.Neuroscience and biobehavioral reviews · 2018Review
- Absence of ALOX5 gene prevents stress-induced memory deficits, synaptic dysfunction and tauopathy in a mouse model of Alzheimer's disease.Human molecular genetics · 2014Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Brain concussions are a serious public concern and are associated with neuropsychiatric disorders, such as depression. Patients with concussion who suffer from depression often experience distress. Nevertheless, few pre-clinical studies have examined concussion-induced depression, and there is little information regarding its pharmacological management. Edaravone, a free radical scavenger, can exert neuroprotective effects in several animal models of neurological disorders. However, the effectiveness of edaravone in animal models of concussion-induced depression remains unclear. In this study, we examined whether edaravone could prevent concussion-induced depression. Mice were subjected to a weight-drop injury and intravenously administered edaravone (3.0 mg/kg) or vehicle immediately after impact. Serial magnetic resonance imaging showed no abnormalities of the cerebrum on diffusion T1- and T2-weighted images. We found that edaravone suppressed concussion-induced depressive-like behavior in the forced swim test, which was accompanied by inhibition of increased hippocampal and cortical oxidative stress (OS) and suppression of 5-lipoxygenase (5-LOX) translocation to the nuclear envelope in hippocampal astrocytes. Hippocampal OS in concussed mice was also prevented by the nicotinamide adenine dinucleotide phosphate oxidase inhibitor, apocynin, and administration of BWB70C, a 5-LOX inhibitor, immediately and 24 h after injury prevented depressive-like behaviors in concussed mice. Further, antidepressant effects of edaravone were observed in mice receiving 1.0 or 3.0 mg/kg of edaravone immediately after impact, but not at a lower dose of 0.1 mg/kg. This antidepressant effect persisted up to 1 h after impact, whereas edaravone treatment at 3 h after impact had no effect on concussion-induced depressive-like behavior. These results suggest that edaravone protects against concussion-induced depression, and this protection is mediated by suppression of OS and 5-LOX translocation.
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