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Journal ArticleDOI

Erythropoietin protects against brain ischemic injury by inhibition of nitric oxide formation.

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TLDR
In vivo recombinant human erythropoietin effects on brain ischemic injury could be due to inhibition of NO overproduction, as indicated by reduction in nitrite and nitrate in the hippocampus, as observed after ischemia.
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This article is published in European Journal of Pharmacology.The article was published on 2000-08-11. It has received 246 citations till now. The article focuses on the topics: Erythropoietin & Brain ischemia.

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Citations
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Journal ArticleDOI

Erythropoietin prevents motor neuron apoptosis and neurologic disability in experimental spinal cord ischemic injury.

TL;DR: Clinical trials evaluating rHu-EPO's potential to prevent motor neuron apoptosis and the neurological deficits that occur as a consequence of ischemic injury are warranted.
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Erythropoietin Is a Paracrine Mediator of Ischemic Tolerance in the Brain: Evidence from an In Vitro Model

TL;DR: The results establish EPO as an important paracrine neuroprotective mediator of ischemic preconditioning and provide evidence for the following signaling cascade: HIF-1 is activated rapidly by hypoxia in astrocytes and EPO activates the neuronal EPO receptor and, subsequently, JAK-2 and thereby PI3K.
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Recombinant human erythropoietin counteracts secondary injury and markedly enhances neurological recovery from experimental spinal cord trauma.

TL;DR: Observations suggest that rhEPO provides early recovery of function, especially after spinal cord compression, as well as longer-latency neuroprotective, antiinflammatory and antiapoptotic functions.
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Normobaric hypoxia induces tolerance to focal permanent cerebral ischemia in association with an increased expression of hypoxia-inducible factor-1 and its target genes, erythropoietin and VEGF, in the adult mouse brain.

TL;DR: The authors' findings show that hypoxia elicits a delayed, short-lasting (<72 hours) tolerance to focal permanent ischemia in the adult mouse brain, and this model might be a useful paradigm to further study the mechanisms of ischemic tolerance, to identify new therapeutic targets for stroke.
References
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Journal ArticleDOI

Apparent hydroxyl radical production by peroxynitrite: implications for endothelial injury from nitric oxide and superoxide.

TL;DR: It is proposed that superoxide dismutase may protect vascular tissue stimulated to produce superoxide and NO under pathological conditions by preventing the formation of peroxynitrite.
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Temporal profile of neuronal damage in a model of transient forebrain ischemia.

TL;DR: The unique delay in onset of ischemic cell change and the protracte increase in its incidence between 24 and 72 hours could reflect either delayed‐appearance of isChemic change in previously killed neurons or a delayed insult that continued to jeopardize compromised but otherwise viable neurons during the postischemic period.
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Bright and dark sides of nitric oxide in ischemic brain injury

TL;DR: Defining the role of NO in cerebral ischemia provides the rationale for new neuroprotective strategies based on modulation of NO production in the post-ischemic brain.
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In vivo evidence that erythropoietin protects neurons from ischemic damage.

TL;DR: In vivo evidence is reported that EPO protects neurons against ischemia-induced cell death and may exert its neuroprotective effect by reducing the NO-mediated formation of free radicals or antagonizing their toxicity.
Journal ArticleDOI

Endogenous nitric oxide synthesis: Biological functions and pathophysiology

TL;DR: NO appears to play a major role in the pathophysiology of stroke, Parkinson's disease, Huntington's disease and amyotrophic lateral sclerosis, and in the brain, NO functions as a neuromodulator and appears to mediate aspects of learning and memory.
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