2000
DOI: 10.1016/s0014-2999(00)00081-9
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In vivo evidence that erythropoietin has a neuroprotective effect during subarachnoid hemorrhage

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Cited by 75 publications
(47 citation statements)
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“…42 Epo acts as the main regulator of proliferation and differentiation of erythroid progenitor cells in the bone marrow. 13 Neuroprotective effects of systemically administered Epo have been shown in animal models of focal cerebral ischemia, traumatic brain injury, subarachnoid hemorrhage, and spinal cord injury, 19,[43][44][45] but the relevance of the underlying molecular mechanisms in vivo remained still unclear. Additionally, Epo treatment rescued RGCs from apoptosis in a retinal ischemia model and improved RGC function determined by ERG recordings.…”
Section: Discussionmentioning
confidence: 99%
“…42 Epo acts as the main regulator of proliferation and differentiation of erythroid progenitor cells in the bone marrow. 13 Neuroprotective effects of systemically administered Epo have been shown in animal models of focal cerebral ischemia, traumatic brain injury, subarachnoid hemorrhage, and spinal cord injury, 19,[43][44][45] but the relevance of the underlying molecular mechanisms in vivo remained still unclear. Additionally, Epo treatment rescued RGCs from apoptosis in a retinal ischemia model and improved RGC function determined by ERG recordings.…”
Section: Discussionmentioning
confidence: 99%
“…The close association between EPO and blood-related processes originally provoked a primary research focus around the use of EPO in vascular brain injury (e.g. Alafaci et al, 2000;Brines et al, 2000;Buemi et al, 2000;Calapai et al, 2000;Grasso, 2001;Siren et al, 2001;Springborg et al, 2002). Subsequently, however, it turned out that EPO possesses a strong therapeutic potential even in TBI -including the ability to reduce posttraumatic cognitive impairments and support the cognitive rehabilitative processes (e.g.…”
Section: Supporting the Posttraumatic Rehabilitative Processmentioning
confidence: 99%
“…In particular, analysis of cortical neurons showed that the EPOtreated rabbits presented with a significant decrease in the amount of necrotic neurons compared with the untreated and placebo-treated animals (80). Another outcome, and prevents brain ischemic damage (37,38,(80)(81)(82)(83)(84)(85)(86)(87)(88). Given these findings, and according to reports that have demonstrated that EPO enhances the NO system activity (27,68,69), and neuroprotective effects on cerebral cortical neurons from N-methyl-d-aspartate receptormediated glutamate toxicity (71), we further investigated the potential protective effects of rHuEPO in a rabbit model of SAH.…”
Section: From Bench To Bedsidementioning
confidence: 99%