The use of antioxidants in the treatment of traumatic brain injury

Venegoni, Whitney; Shen, Qiuhua; Thimmesch, Amanda R.; Bell, Meredith; Hiebert, John M.; Pierce, Janet D.

doi:10.1111/jan.13259

Cited by 18 publications

(19 citation statements)

References 43 publications

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“…The oxidative stress response to TBI has also been shown to affect cerebral blood flow, and thereby directly correlates with cerebral perfusion and oxygenation of brain tissue (23, 24). Unfortunately, the production of ROS following TBI is heterogeneous and unregulated, making it difficult to assess the isolated impact of oxidative stress on cerebral blood flow after injury in vivo (25). The sources of oxidative stress following TBI are multiple including cellular and molecular pathways occurring in various cell types such as activated endothelial cells, astrocytes, and microglia, as well as damaged neurons.…”

Section: Brain Injury Mechanisms: Inflammation and Oxidative Stressmentioning

confidence: 99%

Endothelial Targeted Strategies to Combat Oxidative Stress: Improving Outcomes in Traumatic Brain Injury

et al. 2019

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The endothelium is a thin monolayer of specialized cells that lines the luminal wall of blood vessels and constitutes the critical innermost portion of the physical barrier between the blood and the brain termed the blood-brain barrier (BBB). Aberrant changes in the endothelium occur in many neuropathological states, including those with high morbidity and mortality that lack targeted therapeutic interventions, such as traumatic brain injury (TBI). Utilizing ligands of surface determinants expressed on brain endothelium to target and combat injury mechanisms at damaged endothelium offers a new approach to the study of TBI and new avenues for clinical advancement. Many factors influence the targets that are expressed on endothelium. Therefore, the optimization of binding sites and ideal design features of nanocarriers are controllable factors that permit the engineering of nanotherapeutic agents with applicability that is specific to a known disease state. Following TBI, damaged endothelial cells upregulate cell adhesion molecules, including ICAM-1, and are key sites of reactive oxygen species (ROS) generation, including hydrogen peroxide. Reactive oxygen species along with pro-inflammatory mediators are known to contribute to endothelial damage and loss of BBB integrity. The use of targeted endothelial nanomedicine, with conjugates of the antioxidant enzyme catalase linked to anti-ICAM-1 antibodies, has recently been demonstrated to minimize oxidative stress at the BBB and reduce neuropathological outcomes following TBI. Here, we discuss targeted endothelial nanomedicine and its potential to provide benefits in TBI outcomes and future directions of this approach.

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Section: Brain Injury Mechanisms: Inflammation and Oxidative Stressmentioning

confidence: 99%

Endothelial Targeted Strategies to Combat Oxidative Stress: Improving Outcomes in Traumatic Brain Injury

et al. 2019

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“…The antioxidant therapy is a strategy whose purpose is the use of complementary antioxidants that could sweep away free radicals. 4,15 Given the great evidence of the high morbidity and mortality rates of TBI, as aforementioned, it is more valuable to have measures or therapeutic strategies that allow us to have preventive procedures which could reduce the symptoms and neurological injuries as a result of the trauma. Research studies provide evidence that mitochondrial dysfunction plays a dominant role in the pathophysiology of TBI, Management Strategies for Mitochondrial Dysfunction in Traumatic Brain Injury Bonilla-Mendoza et al…”

Section: Management Strategiesmentioning

confidence: 99%

“…14 There are some management strategies which have shown a great influence in the outcome of individuals, among them Coenzyme Q10, the most powerful, demonstrates an effective reduction of oxidative stress. 4,15 An important endogenous antioxidant is ubiquinol, a reduced form of coenzyme Q10 stabilizes the membranes, especially the inner mitochondrial membrane which prevents mitochondrial dysfunction by stabilizing them. It also improves energy production and biogenesis processes, as well as inhibit cell death through mitochondrial pathways.…”

Section: Target Moleculesmentioning

confidence: 99%

“…It also improves energy production and biogenesis processes, as well as inhibit cell death through mitochondrial pathways. 15 N-acetyl cysteine is another molecule which possesses antiapoptotic properties, and improves mitochondrial energy by increasing glutathione. 2,4 Another interesting strategy is cyclosporin A (CsA), which has been shown to inhibit the increase of mitochondrial permeability and decrease the formation of free radicals.…”

Section: Target Moleculesmentioning

confidence: 99%

“…18 Contemplating the functions could be a complementary treatment to reduce the severity of secondary injury after trauma. 15,18…”

Section: Target Moleculesmentioning

confidence: 99%

See 2 more Smart Citations

Mitochondrial Dysfunction in Traumatic Brain Injury: Management Strategies

Bonilla-Mendoza

García-Ballestas

Pacheco-Hernández

et al. 2020

Indian Journal of Neurotrauma

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Today, traumatic brain injuries continue to be studied, increasingly investigating the pathophysiological mechanisms that contribute to the clinical presentation, severity, and possible sequelae, but despite this, the prognosis of these patients is sometimes poor. Mitochondrial dysfunction comprises a series of reactions that contribute to the inflammatory process in these patients that have an impact on the prognosis, since it is one of the pathophysiological mechanisms involved in secondary lesions after a traumatic brain injury; and therefore has opened a field of study in the search of possible biomolecular markers that allow us to establish a prognosis and prediction of mortality.

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