Erythropoietin neuroprotection with traumatic brain injury

Ponce, Lucido L.; Navarro, Jovany Cruz; Ahmed, Osama; Robertson, Claudia S.

doi:10.1016/j.pathophys.2012.02.005

Cited by 69 publications

(57 citation statements)

References 83 publications

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“…Furthermore, the secreted EPO could bind to the EPO receptors present on neuronal membranes nearby. Furthermore, EPO could also protect the nerves from secondary brain damage after TBI by relieving cerebrum edema [11], facilitating neuronal regeneration [12], lowering toxicity of excitatory amino acid neurotransmitters [13], and playing anti-oxidative effect [14]. Our present study used the r-HuEPO to treat traumatic brain injury in rats, and explore the effects of r-HuEPO on the expressions of NF-kB, c-myc and Fas/Fasl in brain tissue.…”

Section: Introductionmentioning

confidence: 90%

Effect of recombinant human erythropoietin expressions of apoptosis genes in rats following traumatic brain injury

Yuan¹,

Bian²,

Wei³

et al. 2016

Trop. J. Pharm Res

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Section: Introductionmentioning

confidence: 90%

Effect of recombinant human erythropoietin expressions of apoptosis genes in rats following traumatic brain injury

Yuan¹,

Bian²,

Wei³

et al. 2016

Trop. J. Pharm Res

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“…Numerous experimental studies in recent years have suggested that erythropoietin (EPO) is an endogenous mediator of neuroprotection in various central nervous system disorders, including TBI (18). Erythropoietin is a glycoprotein and cytokine of 34kDa which is produced mainly by the fetal liver and the adult kidney in response to hypoxia.…”

Section: Antioxidant Therapeutic Strategiesmentioning

confidence: 99%

“…The blockade of oxidative damage seems to be a rational intervention to reduce secondary brain injury after TBI, and establishing the time course of oxidative damage provides information on a possible therapeutic window for protection against secondary brain injury (1,17,18). Therefore, to find pharmacological agents specifically aiming to inhibit oxidative stress and modifying the expression of inflammatory cytokines might be a critical strategy; thus, antioxidants have been a major point for consideration (19).…”

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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“…46 Several studies have demonstrated that EPO shows antiexcitotoxic, antioxidant, antiedematous, and antiinflammatory effects in TBI. [47][48][49][50] Brain injury causes upregulation of EpoR expression. 45 Reduced number of neural progenitor cells (NPCs) and increased apoptosis has been found in the mice lacking the EPO receptor.…”

Section: 34mentioning

confidence: 99%

“…51 EPO/EpoR signal pathway has been shown to be involved in neuroprotection in pathological conditions. 50,52 Expression of the receptors for EPO is significantly increased in neurons, glia, and endothelial cells after TBI. 41 EPO appears to promote neuroprotection through binding to EpoR and activating JAK-2/NF-kB and PI3K signaling pathway.…”

Section: 34mentioning

confidence: 99%

Traumatic Brain Injury: Current Treatment Strategies and Future Endeavors

2016

Cell Transplant

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Traumatic brain injury (TBI) presents in various forms ranging from mild alterations of consciousness to an unrelenting comatose state and death. In the most severe form of TBI, the entirety of the brain is affected by a diffuse type of injury and swelling. Treatment modalities vary extensively based on the severity of the injury and range from daily cognitive therapy sessions to radical surgery such as bilateral decompressive craniectomies. Guidelines have been set forth regarding the optimal management of TBI, but they must be taken in context of the situation and cannot be used in every individual circumstance. In this review article, we have summarized the current status of treatment for TBI in both clinical practice and basic research. We have put forth a brief overview of the various subtypes of traumatic injuries, optimal medical management, and both the noninvasive and invasive monitoring modalities, in addition to the surgical interventions necessary in particular instances. We have overviewed the main achievements in searching for therapeutic strategies of TBI in basic science. We have also discussed the future direction for developing TBI treatment from an experimental perspective. Keywords traumatic brain injury, management, intracranial hypertension, treatment strategies Epidemiology of Traumatic Brain Injury (TBI)TBI continues to plague millions of individuals around the world on an annual basis. According to the Centers for Disease Control, the total combined rates for TBI-related emergency department visits, hospitalizations, and deaths have increased in the decade 2001-2010. 1 However, taken individually, the number of deaths related to TBIs has decreased over this same period of time likely secondary in part to increased awareness, structuralizing management and guidelines, and significant technological advancements in current treatment regimens. We should also acknowledge that there is a certain percentage of TBIs that never reach medical care, hence, the overall rates for TBIs are likely underreported. 2The highest rates of TBI tend to be in a very young agegroup (0-4 y) as well as in adolescents and young adults (15-24 y). There is another peak in incidence in the elderly (>65 y). The 2 leading causes of TBI overall are falls and motor vehicle accidents.3 As a result of an overall increased number of TBIs, but lower rate of related deaths, we have a growing population of individuals living with significant disabilities directly related to their TBI. Pathophysiology of TBITBI pathogenesis is a complex process that results from primary and secondary injuries that lead to temporary or permanent neurological deficits. The primary deficit is related directly to the primary external impact of the brain. The secondary injury can happen from minutes to days from the primary impact and consists of a molecular, chemical, and inflammatory cascade responsible for further cerebral damage. This cascade involves depolarization of the neurons

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Erythropoietin neuroprotection with traumatic brain injury

Cited by 69 publications

References 83 publications

Effect of recombinant human erythropoietin expressions of apoptosis genes in rats following traumatic brain injury

Effect of recombinant human erythropoietin expressions of apoptosis genes in rats following traumatic brain injury

Antioxidant therapies in traumatic brain injury: a review

Traumatic Brain Injury: Current Treatment Strategies and Future Endeavors

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