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The Anti-Inflammatory and Neuroprotective Effects of Ghrelin in Subarachnoid Hemorrhage-Induced Oxidative Brain Damage in Rats

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dc.contributor.authorVELİOĞLU ÖĞÜNÇ, AYLİZ
dc.contributor.authorsErsahin, Mehmet; Toklu, Hale Z.; Erzik, Can; Cetinel, Sule; Akakin, Dilek; Velioglu-Ogunc, Ayliz; Tetik, Sermin; Ozdemir, Zarife N.; Sener, Goeksel; Yegen, Berrak C.
dc.date.accessioned2022-03-12T17:47:52Z
dc.date.available2022-03-12T17:47:52Z
dc.date.issued2010
dc.description.abstractTo elucidate the putative neuroprotective effects of ghrelin in subarachnoid hemorrhage (SAH)- induced brain injury, Wistar albino rats (n=54) were divided into sham-operated control, saline-treated SAH, and ghrelin-treated (10 mu g/kg/d IP) SAH groups. The rats were injected with blood (0.3mL) into the cisterna magna to induce SAH, and were sacrificed 48 h after the neurological examination scores were recorded. In plasma samples, neuron-specific enolase (NSE), S-100 beta protein, TNF-alpha, and IL-1 beta levels were evaluated, while forebrain tissue samples were taken for the measurement of malondialdehyde (MDA), glutathione (GSH), reactive oxygen species levels, myeloperoxidase (MPO), Na+-K+-ATPase activity, and DNA fragmentation ratio. Brain tissue samples containing the basilar arteries were obtained for histological examination, while cerebrum and cerebellum were removed for the measurement of blood-brain barrier (BBB) permeability and brain water content. The neurological scores were impaired at 48 h after SAH induction, and SAH caused significant decreases in brain GSH content and Na+-K+-ATPase activity, and increases in chemiluminescence, MDA levels, and MPO activity. Compared with the control group, the protein levels of NSE, S-100 beta, TNF-alpha, and IL-1 beta in plasma were also increased, while ghrelin treatment prevented all SAH-induced alterations observed both biochemically and histopathologically. The results demonstrate that ghrelin alleviates SAH-induced oxidative brain damage, and exerts neuroprotection by maintaining a balance in oxidant-antioxidant status, by inhibiting proinflammatory mediators, and preventing the depletion of endogenous antioxidants evoked by SAH.
dc.identifier.doi10.1089/neu.2009.1210
dc.identifier.eissn1557-9042
dc.identifier.issn0897-7151
dc.identifier.pubmed20205513
dc.identifier.urihttps://hdl.handle.net/11424/229850
dc.identifier.wosWOS:000278933300017
dc.language.isoeng
dc.publisherMARY ANN LIEBERT, INC
dc.relation.ispartofJOURNAL OF NEUROTRAUMA
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectcerebral vasospasm
dc.subjectghrelin
dc.subjectlipid peroxidation
dc.subjectneuron-specific enolase
dc.subjectoxidative stress
dc.subjectsubarachnoid hemorrhage
dc.subjectS-100 beta
dc.subjectNEURON-SPECIFIC ENOLASE
dc.subjectREMOTE ORGAN INJURY
dc.subjectCEREBRAL VASOSPASM
dc.subjectCEREBROSPINAL-FLUID
dc.subjectHEAD-INJURY
dc.subjectISCHEMIA-REPERFUSION
dc.subjectRADICAL SCAVENGER
dc.subjectACYLATED PEPTIDE
dc.subjectREACTIVE OXYGEN
dc.subjectPROTEIN S-100B
dc.titleThe Anti-Inflammatory and Neuroprotective Effects of Ghrelin in Subarachnoid Hemorrhage-Induced Oxidative Brain Damage in Rats
dc.typearticle
dspace.entity.typePublication
local.avesis.idece33de9-32c0-45a6-a1cb-307245f19e5d
local.import.packageSS17
local.indexed.atWOS
local.indexed.atSCOPUS
local.journal.numberofpages13
oaire.citation.endPage1155
oaire.citation.issue6
oaire.citation.startPage1143
oaire.citation.titleJOURNAL OF NEUROTRAUMA
oaire.citation.volume27
relation.isAuthorOfPublication13300bf6-ba96-4f87-9868-b0d2c86f572a
relation.isAuthorOfPublication.latestForDiscovery13300bf6-ba96-4f87-9868-b0d2c86f572a

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