Neuroprotective effect of cinnamaldehyde on secondary brain injury after traumatic brain injury in a rat model
dc.authorid | Bora Gürer / 0000-0003-1500-6184 | |
dc.authorscopusid | Bora Gürer / 36448801100 | |
dc.authorwosid | Bora Gürer / JIJ-1874-2023 | |
dc.contributor.author | Kuru Bektaşoğlu, Pınar | |
dc.contributor.author | Koyuncuoğlu, Türkan | |
dc.contributor.author | Demir, Dilan | |
dc.contributor.author | Sucu, Gizem | |
dc.contributor.author | Akakın, Dilek | |
dc.contributor.author | Peker Eyüboğlu, İrem | |
dc.contributor.author | Yüksel, Meral | |
dc.contributor.author | Çelikoğlu, Erhan | |
dc.contributor.author | Yeğen, Berrak Ç. | |
dc.date.accessioned | 2021-08-02T07:08:15Z | |
dc.date.available | 2021-08-02T07:08:15Z | |
dc.date.issued | 2021 | en_US |
dc.department | İstinye Üniversitesi, Tıp Fakültesi, Cerrahi Tıp Bilimleri Bölümü | en_US |
dc.description.abstract | Objective: The aim of this study was to investigate the possible neuroprotective effects of cinnamaldehyde (CA) on secondary brain injury after traumatic brain injury (TBI) in a rat model. Methods: Rats were randomly divided into 4 groups: control (n = 9), TBI (n = 9), vehicle (0.1% Tween 80; n = 8), and CA (100 mg/kg) (n = 9). TBI was induced by the weight-drop model. In brain tissues, myeloperoxidase activity and the levels of luminol-enhanced and lucigenin-enhanced chemiluminescence were measured. Interleukin 1?, interleukin 6, tumor necrosis factor ?, tumor growth factor ?, caspase-3, and cleaved caspase-3 were evaluated with an enzyme-linked immunosorbent assay method. Brain injury was histopathologically graded after hematoxylin-eosin staining. Y-maze and novel object recognition tests were performed before TBI and within 24 hours of TBI. Results: Higher myeloperoxidase activity levels in the TBI group (P < 0.001) were suppressed in the CA group (P < 0.05). Luminol-enhanced and lucigenin-enhanced chemiluminescence, which were increased in the TBI group (P < 0.001, for both), were decreased in the group that received CA treatment (P < 0.001 for both). Compared with the increased histologic damage scores in the cerebral cortex and dentate gyrus of the TBI group (P < 0.001), scores of the CA group were lower (P < 0.001). Decreased number of entries and spontaneous alternation percentage in the Y-maze test of the TBI group (P < 0.05 and P < 0.01, respectively) were not evident in the CA group. Conclusions: CA has shown neuroprotective effects by limiting neutrophil recruitment, suppressing reactive oxygen species and reducing histologic damage and acute hippocampal dysfunction. | en_US |
dc.identifier.citation | Bektaşoğlu, P. K., Koyuncuoğlu, T., Demir, D., Sucu, G., Akakın, D., Eyüboğlu, İ. P., ... & Gürer, B. (2021). Neuroprotective Effect of Cinnamaldehyde on The Secondary Brain Injury Seen After Traumatic Brain Injury in a Rat Model. World Neurosurgery. | en_US |
dc.identifier.doi | 10.1016/j.wneu.2021.06.117 | en_US |
dc.identifier.issn | 1878-8750 | en_US |
dc.identifier.pmid | 34224887 | en_US |
dc.identifier.scopus | 2-s2.0-85110707326 | en_US |
dc.identifier.scopusquality | Q2 | en_US |
dc.identifier.uri | https://doi.org/10.1016/j.wneu.2021.06.117 | |
dc.identifier.uri | https://hdl.handle.net/20.500.12713/1970 | |
dc.identifier.wos | WOS:000687942800033 | en_US |
dc.identifier.wosquality | Q3 | en_US |
dc.indekslendigikaynak | Web of Science | en_US |
dc.indekslendigikaynak | Scopus | en_US |
dc.indekslendigikaynak | PubMed | en_US |
dc.institutionauthor | Gürer, Bora | |
dc.language.iso | en | en_US |
dc.publisher | Elsevier Inc. | en_US |
dc.relation.ispartof | World Neurosurgery | en_US |
dc.relation.publicationcategory | Makale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı | en_US |
dc.rights | info:eu-repo/semantics/closedAccess | en_US |
dc.subject | Antiinflammatory | en_US |
dc.subject | Antioxidant | en_US |
dc.subject | Cinnamaldehyde | en_US |
dc.subject | Neuroprotection | en_US |
dc.subject | Rat | en_US |
dc.subject | Traumatic Brain Injury | en_US |
dc.title | Neuroprotective effect of cinnamaldehyde on secondary brain injury after traumatic brain injury in a rat model | en_US |
dc.type | Article | en_US |