Publication:
The effects of Cinnamaldehyde on early brain injury and cerebral vasospasm following experimental subarachnoid hemorrhage in rabbits

dc.contributor.authorsGurer, Bora; Kertmen, Hayri; Kuru Bektasoglu, Pinar; Ozturk, Ozden Caglar; Bozkurt, Huseyin; Karakoc, Abdullah; Arikok, Ata Turker; Celikoglu, Erhan
dc.date.accessioned2022-03-12T22:39:19Z
dc.date.accessioned2026-01-10T20:35:22Z
dc.date.available2022-03-12T22:39:19Z
dc.date.issued2019
dc.description.abstractThe neuroprotective and vasodilatory effects of cinnamaldehyde have been widely studied and documented. On the basis of these findings, we hypothesized that cinnamaldehyde exhibits therapeutic effects on subarachnoid hemorrhage-induced early brain injury and cerebral vasospasm. Thirty-two adult male New Zealand white rabbits were randomly divided into four groups of eight rabbits: control, subarachnoid hemorrhage, subarachnoid hemorrhage + vehicle, and subarachnoid hemorrhage + cinnamaldehyde. An intraperitoneal dose of 50 mg/kg cinnamaldehyde was administered 5 min following an intracisternal blood injection, followed by three further daily injections at identical doses. The animals were sacrificed 72 h after subarachnoid hemorrhage was induced. The cross-sectional areas and arterial wall thicknesses of the basilar artery were measured and hippocampal degeneration scores were evaluated. Treatment with cinnamaldehyde was effective in providing neuroprotection and attenuating cerebral vasospasm after subarachnoid hemorrhage in rabbits. It effectively increased the cross-sectional areas of the basilar artery and reduced the arterial wall thickness; in addition, hippocampal degeneration scores were lower in the cinnamaldehyde group. The findings of this study showed, for the first time to our knowledge, that cinnamaldehyde exhibits neuroprotective activity against subarachnoid hemorrhage-induced early brain injury and that it can prevent vasospasm. Potential mechanisms underlying the neuroprotection and vasodilation were discussed. Cinnamaldehyde could play a role in subarachnoid hemorrhage treatment.
dc.identifier.doi10.1007/s11011-019-00480-7
dc.identifier.eissn1573-7365
dc.identifier.issn0885-7490
dc.identifier.pubmed31444631
dc.identifier.urihttps://hdl.handle.net/11424/235803
dc.identifier.wosWOS:000496665000019
dc.language.isoeng
dc.publisherSPRINGER/PLENUM PUBLISHERS
dc.relation.ispartofMETABOLIC BRAIN DISEASE
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectCinnamaldehyde
dc.subjectEarly brain injury
dc.subjectNeuroprotection
dc.subjectRabbit
dc.subjectSubarachnoid hemorrhage
dc.subjectVasospasm
dc.subjectREDUCING OXIDATIVE STRESS
dc.subjectROOT GANGLION NEURONS
dc.subjectKAPPA-B
dc.subjectPOTENTIAL CONTRIBUTION
dc.subjectTRANS-CINNAMALDEHYDE
dc.subjectCALCIUM-CHANNELS
dc.subjectRAT
dc.subjectMECHANISMS
dc.subjectACTIVATION
dc.subjectREDUCTION
dc.titleThe effects of Cinnamaldehyde on early brain injury and cerebral vasospasm following experimental subarachnoid hemorrhage in rabbits
dc.typearticle
dspace.entity.typePublication
oaire.citation.endPage1746
oaire.citation.issue6
oaire.citation.startPage1737
oaire.citation.titleMETABOLIC BRAIN DISEASE
oaire.citation.volume34

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