Superoxide Dismutase, Catalase, and Guanase in Traumatic Brain Injury

Kuçur, Mine; Tanrıverdi, Taner; Dashti, Reza; Höhn, Anne Kathrin; Yentür, Ercüment; Belce, Ahmet; Uzan, Mustafa; Kaynar, Mehmet Yaşar

doi:10.1097/01.wnq.0000173450.16339.77

Cited by 4 publications

(4 citation statements)

References 29 publications

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“…These analyses showed the presence of classical neurotrophins and neuroprotective cytokines including BDNF, EGF, HGF, VEGF, PDGF, a neuron and glial growth regulator (glia maturation factor beta), 29 less known neuroprotective factors (TIMP-1, Neurabin-2 etc. ), antioxidative agents (catalase, glutathione S-transferases, SOD, guanase), 30 and anti-inflammatory molecules TGF-β, fibroblast growth factor (FGF), insulin-like growth factor (IGF), etc. This is in line with previous characterization of the HPPL by ELISA that established its high contents of neurotrophic, angiogenic, and anti-inflammatory growth factors such as PDGF, BDNF, β-FGF, VEGF, and TGF-β1.…”

Section: Discussionmentioning

confidence: 99%

Human platelet lysate biotherapy for traumatic brain injury: preclinical assessment

Nebie

Carvalho

Barro

et al. 2021

Brain

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Traumatic brain injury leads to major brain anatomopathological damages underlined by neuroinflammation, oxidative stress and progressive neurodegeneration, ultimately leading to motor and cognitive deterioration. The multiple pathological events resulting from traumatic brain injury can be addressed not by a single therapeutic approach, but rather by a synergistic biotherapy capable of activating a complementary set of signaling pathways and providing synergistic neuroprotective, anti-inflammatory, antioxidative, and neurorestorative activities. Human platelet lysate might fulfill these requirements as it is comprised of a plethora of biomolecules readily accessible as a traumatic brain injury biotherapy. In the present study, we have tested the therapeutic potential of human platelet lysate using in vitro and in vivo models of traumatic brain injury. We first prepared and characterized platelet lysate from clinical-grade human platelet concentrates. Platelets were pelletized, lysed by three freeze-thaw cycles, and centrifuged. The supernatant was purified by 56 °C-30 minutes heat-treatment and spun to obtain the heat-treated platelet pellet lysate that was characterized by ELISA and proteomic analyses. Two mouse models were used to investigate platelet lysate neuroprotective potential. The injury was induced by an in-house manual controlled scratching of the animals' cortex or by controlled cortical impact injury. The platelet lysate treatment was performed by topical application of 60 µL in the lesioned area, followed by daily 60 µL intranasal administration from day 1 to 6 post-injury. Platelet lysate proteomics identified over 1000 proteins including growth factors, neurotrophins, and antioxidants. ELISA detected several neurotrophic and angiogenic factors at ca. 1–50 ng/mL levels. We demonstrate, using the two mouse models of traumatic brain injury that topical application and intranasal platelet lysate consistently improved mice motor function in the beam and rotarod tests, mitigated cortical neuroinflammation, and oxidative stress in the injury area, as revealed by downregulation of pro-inflammatory genes and the reduction in reactive oxygen species levels. Moreover, platelet lysate treatment reduced the loss of cortical synaptic proteins. Unbiased proteomic analyses revealed that HPPL reversed several pathways promoted by both CCI and CBS and related to transport, post-synaptic density, mitochondria or lipid metabolism. The present data strongly support for the first time that human platelet lysate is a reliable and effective therapeutic source of neurorestorative factors. Therefore, brain administration of platelet lysate is a therapeutical strategy that deserves serious and urgent consideration for universal brain trauma treatment.

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Section: Discussionmentioning

confidence: 99%

Human platelet lysate biotherapy for traumatic brain injury: preclinical assessment

Nebie

Carvalho

Barro

et al. 2021

Brain

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“…However, there is an increasing trend of SOD and catalase proportional to the severity of head trauma, indicating the presence of SOD interactions and catalase as antioxidant enzymes with ROS for cell protection. 20 Damage to brain tissue due to head trauma was also related to the demyelination process, which causes long-term cognitive deficits and sensorimotor. Oligodendrocytes as the primary cells responsible for producing and maintaining the myelin membranes under normal conditions and remyelination after axonal damage are highly sensitive to both ischemic and traumatic situations.…”

Section: Original Articlementioning

confidence: 99%

The oxidative-stress level determine patientâ€™s outcomes with a severe head injury at Sanglah General Hospital, Denpasar, Indonesia

Wirawan¹,

Golden²,

Niryana³

2019

Intisari Sains Medis

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Background: In secondary brain injury, oxidative stress will occur due to a balance disorder between pro-oxidants with antioxidants. The antioxidant activity that is often used to assess oxidative stress, such as malondialdehyde (MDA), is superoxide dismutase (SOD) and glutathione peroxidase (GPx). This study aims to evaluate the level of oxidative stress, reflected by the MDA serum level and SOD level to determine the outcomes of patients with severe head injury. Method: A cross-sectional analytic study was conducted among 40 patients with severe head injury within 24 hours post-trauma at Emergency Ward, Surgery Department, Sanglah General Hospital Denpasar from January-June 2017. MDA and SOD levels were assessed using ELISA at Clinical Pathology Laboratory, Sanglah General Hospital. Data were analyzed using SPSS ver. 16 software. Results: This study found significant differences on elevated MDA levels (p-value < 0.05) in patients who died or had a persistent vegetative state, patients with severe disability and those with a good recovery/moderate disability. The statistical analysis also found a significant difference in MDA serum levels among patient with severe disability and patients with a good recovery/moderate disability (P=0,028). Meanwhile, there was no significant correlation between SOD serum levels and patients outcome (P>0.05). Conclusion: Increased MDA serum levels is a significant factor in predicting outcomes of patients with severe head injury.

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“…Their study also reported a concomitant increase in stress proteins, known to trigger inflammation, signifying the role of SOD and CAT in neuroprotection against oxidative stress. The high levels of unsaturated lipids and fatty acids present in neuronal cells make them highly susceptible to oxidative damage (74). …”

Section: Drugs and Drug Delivery Systemsmentioning

confidence: 99%

Drug delivery, cell-based therapies, and tissue engineering approaches for spinal cord injury

Kabu

Gao

Kwon

et al. 2015

Journal of Controlled Release

168

114

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Spinal cord injury (SCI) results in devastating neurological and pathological consequences, causing major dysfunction to the motor, sensory and autonomic systems. The primary traumatic injury to the spinal cord triggers a cascade of acute and chronic degenerative events, leading to further secondary injury. Many therapeutic strategies have been developed to potentially intervene in these progressive neurodegenerative events and minimize secondary damage to the spinal cord. Additionally, significant efforts have been directed towards regenerative therapies that may facilitate neuronal repair and establish connectivity across the injury site. Despite the promise that these approaches have shown in preclinical animal models of SCI, challenges with respect to successful clinical translation still remain. The factors that could have contributed to failure include important biologic and physiologic differences between the preclinical models and the human condition, study designs that do not mirror clinical reality, discrepancies in dosing and the timing of therapeutic interventions, and dose-limiting toxicity. With a better understanding of the pathobiology of events following acute SCI, developing integrated approaches aimed at preventing secondary damage and also facilitating neurodegenerative recovery is possible, and hopefully will lead to effective treatments for this devastating injury. The focus of this review is to highlight the progress that has been made in drug therapies and delivery systems, and also cell-based and tissue engineering approaches for SCI.

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Superoxide Dismutase, Catalase, and Guanase in Traumatic Brain Injury

Cited by 4 publications

References 29 publications

Human platelet lysate biotherapy for traumatic brain injury: preclinical assessment

Human platelet lysate biotherapy for traumatic brain injury: preclinical assessment

The oxidative-stress level determine patientâ€™s outcomes with a severe head injury at Sanglah General Hospital, Denpasar, Indonesia

Drug delivery, cell-based therapies, and tissue engineering approaches for spinal cord injury

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