The effects of L-arginine on neurological function, histopathology, and expression of hypoxia-inducible factor-1 alpha following spinal cord ischemia in rats

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dc.contributor.authorTuncer, MC
dc.contributor.authorHatipoglu, ES
dc.contributor.authorOzturk, H
dc.contributor.authorKervancioglu, P
dc.contributor.authorBuyukbayram, H
dc.date.accessioned2024-04-24T17:14:27Z
dc.date.available2024-04-24T17:14:27Z
dc.date.issued2005
dc.departmentDicle Üniversitesien_US
dc.description.abstractThe aim of this study was to investigate the effects of L-arginine (L-Arg) on neurological function, histopathology, and expression of hypoxia-inducible factor-1 alpha (HIF-1 alpha) following spinal cord ischemia in rats, and the interaction between therapy with the nitric oxide donor L-Arg and up-regulation of the expression of HIF-1 alpha. Thirty Wistar rats weighing between 200 and 250 g were divided into three groups, each containing 10 rats: group 1, sham operation; group 2, untreated ischemia-reperfusion (I-R); group 3, I-R plus L-Arg treatment. Spinal cord ischemia was applied for 20 min. There were no significant differences in mean arterial pressures, temperatures, and blood gas levels among the groups. In group 2, malondialdehyde values were significantly increased compared with groups 1 and 3. The rats with aortic occlusion in group 2 had paraplegia or paraparesis. In group 3, all animals were neurologically intact. In group 3, spinal motor neurons did not decrease significantly, and little proliferation of microglia was observed compared with those in group 2. In group 2, spinal motor neurons in ventral gray matter decreased significantly compared with those in groups 1 and 3. HIF-1 alpha-positive immunostaining was mildly detected in group 2 animals. The expression of immunoreactive cells was intensely increased in spinal cord tissue from I-R/L-Arg rats. In conclusion, our findings suggest that HIF-1 alpha-positive immunostaining may be critical factors in the pathophysiology of inflammatory spinal cord injury induced by I-R. Nitric oxide may play an important role in the immunohistochemical expression of these molecules, and the neuroprotective benefit of L-Arg may be attributed to preventing neural cell necrosis. Copyright (C) 2005 S. Karger AG, Basel.en_US
dc.identifier.doi10.1159/000090331
dc.identifier.endpage329en_US
dc.identifier.issn0014-312X
dc.identifier.issn1421-9921
dc.identifier.issue6en_US
dc.identifier.pmid16465055
dc.identifier.scopus2-s2.0-32244434410
dc.identifier.scopusqualityQ2
dc.identifier.startpage323en_US
dc.identifier.urihttps://doi.org/10.1159/000090331
dc.identifier.urihttps://hdl.handle.net/11468/17943
dc.identifier.volume37en_US
dc.identifier.wosWOS:000235209400002
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoenen_US
dc.publisherKargeren_US
dc.relation.ispartofEuropean Surgical Research
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectSpinal Corden_US
dc.subjectIschemia And Reperfusion Injuryen_US
dc.subjectHypoxia-Inducible Factor-1 Alphaen_US
dc.subjectL-Arginineen_US
dc.titleThe effects of L-arginine on neurological function, histopathology, and expression of hypoxia-inducible factor-1 alpha following spinal cord ischemia in ratsen_US
dc.titleThe effects of L-arginine on neurological function, histopathology, and expression of hypoxia-inducible factor-1 alpha following spinal cord ischemia in rats
dc.typeArticleen_US

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