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., ...Daha Fazla

WORLD NEUROSURGERY, cilt.153, 2021 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 153
  • Basım Tarihi: 2021
  • Doi Numarası: 10.1016/j.wneu.2021.06.117
  • Dergi Adı: WORLD NEUROSURGERY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, CAB Abstracts, EMBASE, Index Islamicus, MEDLINE, Veterinary Science Database
  • Anahtar Kelimeler: 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
  • Marmara Üniversitesi Adresli: Evet

Özet

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.