Neuroprotective Effect of Cinnamaldehyde on Secondary Brain Injury After Traumatic Brain Injury in a Rat Model.
World Neurosurg. 2021 Sep ;153:e392-e402. Epub 2021 Jul 2. PMID: 34224887
Pınar Kuru Bektaşoğlu
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 1β, interleukin 6, tumor necrosis factor α, tumor growth factor β, 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 24hours 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.