Neuroprotective Effect of Cinnamaldehyde on Secondary Brain Injury After Traumatic Brain Injury in a Rat Model


Bektasoglu P. K. , Koyuncuoglu T. , Demir D., Sucu G., AKAKIN D. , Eyuboglu İ. , ...More

WORLD NEUROSURGERY, vol.153, 2021 (Journal Indexed in SCI) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 153
  • Publication Date: 2021
  • Doi Number: 10.1016/j.wneu.2021.06.117
  • Title of Journal : WORLD NEUROSURGERY
  • Keywords: Antiinflammatory, Antioxidant, Cinnamaldehyde, Neuroprotection, Rat, Traumatic brain injury, ROOT GANGLION NEURONS, NECROSIS-FACTOR-ALPHA, CLOSED-HEAD INJURY, HIGH GLUCOSE, TRANS-CINNAMALDEHYDE, INDUCED DAMAGE, TNF-ALPHA, EXPRESSION, NEUROINFLAMMATION, INTERLEUKIN-1

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 ac-tivity and the levels of luminol-enhanced and lucigenin-enhanced chemiluminescence were measured. Inter-leukin 1b, interleukin 6, tumor necrosis factor a, tumor growth factor b, 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 chem-iluminescence, 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, respec-tively) 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.