Kuru Bektaşoğlu, PınarKoyuncuoğlu, TürkanDemir, DilanSucu, GizemAkakın, DilekPeker Eyüboğlu, İremYüksel, MeralÇelikoğlu, ErhanYeğen, Berrak Ç.2021-08-022021-08-022021Bektaşoğlu, 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.1878-8750https://doi.org/10.1016/j.wneu.2021.06.117https://hdl.handle.net/20.500.12713/1970Objective: 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.eninfo:eu-repo/semantics/closedAccessAntiinflammatoryAntioxidantCinnamaldehydeNeuroprotectionRatTraumatic Brain InjuryArticle34224887WOS:0006879428000332-s2.0-85110707326Q310.1016/j.wneu.2021.06.117Q2