Oxidative Stress in Brain According to Traumatic Brain Injury Intensity

Petronilho, Fabrícia; Feier, Gustavo; Souza, Bruna de; Guglielmi, Cecília; Constantino, Larissa; Walz, Roger; Quevedo, Joao L De; Dal‐Pizzol, Felipe

doi:10.1016/j.jss.2009.04.031

Cited by 47 publications

(49 citation statements)

References 41 publications

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“…Oxidative stress is considered to play a central role as one of the mechanisms underlying secondary brain damage following TBI (Petronilho et al, 2010). Compelling evidence supports a role for antioxidant strategies aimed at decreasing post-traumatic neurological deficits, cerebral edema, and brain lesion volume induced by oxidative stress (Clausen et al, 2008;Eghwrudjakpor and Allison, 2010;Hall et al, 2010).…”

Section: Fig 3 Inhibition Of Astrocyte Activation By Edaravone (A)mentioning

confidence: 99%

“…Oxidative stress, secondary to excitotoxicity and intracellular calcium dysregulation, plays a central role in secondary brain neuronal death, and contributes to many of the aforementioned pathophysiological changes (Petronilho et al, 2010;. Oxidative stress occurs when there is an imbalance between cellular production of free radicals and the intrinsic ability of cells to sequester and eliminate these free radicals (Gilgun-Sherki et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

“…Although additional clinical studies are necessary to verify its efficacy for ischemic stroke patients (Lapchak, 2010), edaravone's scavenging properties may make it a good candidate for TBI treatment because of the role of oxidative stress in the pathophysiology of TBI (Petronilho et al, 2010). Recently, edaravone has been tested for its neuroprotective and antioxidative effects on the brain after TBI both in rat models and in patients (Dohi et al, 2006;Dohi et al, 2007;Itoh et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

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Free-Radical Scavenger Edaravone Treatment Confers Neuroprotection Against Traumatic Brain Injury in Rats

Wang

Zheng

Li³

et al. 2011

Journal of Neurotrauma

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Traumatic brain injury (TBI) is one of the leading causes of neurological disability in young adults. Edaravone, a novel synthetic small-molecule free-radical scavenger, has been shown to have a neuroprotective effect in both animal models of cerebral ischemia and stroke patients; however, the underlying mechanism is poorly understood. In this report, we investigated the potential mechanisms of edaravone treatment in a rat model of TBI. TBI was induced in the right cerebral cortex of male adult rats using Feeney's weight-drop method. Edaravone (0.75, 1.5, or 3 mg/kg) or vehicle (normal saline) was intravenously administered at 2 and 12 h after TBI. Edaravone treatment significantly decreased hippocampal CA3 neuron loss, reduced oxidative stress, and decreased neuronal programmed cell death compared to vehicle treatment. The protective effects of edaravone treatment were also related to the pathology of TBI on non-neuronal cells, as edaravone decreased astrocyte and glial activation. Lastly, edaravone treatment significantly reduced the presence of inflammatory cytokines, cerebral edema, blood-brain barrier (BBB) permeability, and, importantly, neurological deficits following TBI. Our results suggest that edaravone exerts a neuroprotective effect in the rat model of TBI. The likely mechanism is via inhibiting oxidative stress, leading to a decreased inflammatory response and glial activation, and thereby reducing neuronal death and improving neurological function.

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Section: Fig 3 Inhibition Of Astrocyte Activation By Edaravone (A)mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Free-Radical Scavenger Edaravone Treatment Confers Neuroprotection Against Traumatic Brain Injury in Rats

Wang

Zheng

Li³

et al. 2011

Journal of Neurotrauma

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“…In rats subjected to TBI, the extent of oxidative damage was directly proportionate to the severity of the insult (Petronilho et al, 2009;Tavazzi et al, 2005). The total antioxidant reserves of brain homogenates such as tissue concentrations of ascorbate, glutathione, and sulfhydryl proteins were reduced after TBI in rats (Singh et al, 2007).…”

Section: Oxidative Stress In Penetrating Tbimentioning

confidence: 99%

Common biochemical defects linkage between post-traumatic stress disorders, mild traumatic brain injury (TBI) and penetrating TBI

Prasad¹,

Bondy

2015

Brain Research

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AnxietyPsychological damage a b s t r a c t Post-traumatic stress disorder (PTSD) is a complex mental disorder with psychological and emotional components, caused by exposure to single or repeated extreme traumatic events found in war, terrorist attacks, natural or man-caused disasters, and by violent personal assaults and accidents. Mild traumatic brain injury (TBI) occurs when the brain is violently rocked back and forth within the skull following a blow to the head or neck as in contact sports, or when in close proximity to a blast pressure wave following detonation of explosives in the battlefield. Penetrating TBI occurs when an object penetrates the skull and damages the brain, and is caused by vehicle crashes, gunshot wound to the head, and exposure to solid fragments in the proximity of explosions, and other combat-related head injuries. Despite clinical studies and improved understanding of the mechanisms of cellular damage, prevention and treatment strategies for patients with PTSD and TBI remain unsatisfactory. To develop an improved plan for treating and impeding progression of PTSD and TBI, it is important to identify underlying biochemical changes that may play key role in the initiation and progression of these disorders. This review identifies three common biochemical events, namely oxidative stress, chronic inflammation and excitotoxicity that participate in the initiation and progression of these conditions. While these features are separately discussed, in many instances, they overlap. This review also addresses the goal of developing novel treatments and drug regimens, aimed at combating this triad of events common to, and underlying, injury to the brain.

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“…Traumatic brain injury (TBI) still remains one of the leading causes of death and disability, worldwide (1)(2)(3)(4)(5)(6). TBI constitutes a major global health and socio-economic problem with neurobehavioral sequelae contributing to long-term disability (7).…”

Section: Introductionmentioning

confidence: 99%

Antioxidant therapies in traumatic brain injury: a review

Romero-Rivera¹,

Cabeza-Morales²,

Soto-Zarate³

et al. 2017

Romanian Neurosurgery

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Abstract:Oxidative stress constitute one of the commonest mechanism of the secondary injury contributing to neuronal death in traumatic brain injury cases. The oxidative stress induced secondary injury blockade may be considered as to be a good alternative to improve the outcome of traumatic brain injury (TBI) treatment. Due to absence of definitive therapy of traumatic brain injury has forced researcher to utilize unconventional therapies and its roles investigated in the improvement of management and outcome in recent year. Antioxidant therapies are proven effective in many preclinical studies and encouraging results and the role of antioxidant mediaction may act as further advancement in the traumatic brain injury management it may represent aonr of newer moadlaity in neurosurgical aramamentorium, this kind of therapy could be a good alternative or adjuct to the previously established neuroprotection agents in TBI.

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Oxidative Stress in Brain According to Traumatic Brain Injury Intensity

Cited by 47 publications

References 41 publications

Free-Radical Scavenger Edaravone Treatment Confers Neuroprotection Against Traumatic Brain Injury in Rats

Free-Radical Scavenger Edaravone Treatment Confers Neuroprotection Against Traumatic Brain Injury in Rats

Common biochemical defects linkage between post-traumatic stress disorders, mild traumatic brain injury (TBI) and penetrating TBI

Antioxidant therapies in traumatic brain injury: a review

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