Abstract
Aim:
The aim of this study was to investigate the possible neuroprotective effects of Cinnamaldehyde (CA) on the secondary brain injury seen 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- and lucigenin-enhanced chemiluminescence were measured. Interleukin-1β, interleukin-6, tumor necrosis factor-α, tumor growth factor-β, caspase 3, and cleaved caspase 3 was evaluated with enzyme linked immunosorbent assay (ELISA) method. Brain injury was histopathologically graded following hematoxylin-eosin staining. Y-maze and novel object recognition tests were performed before TBI and within the 24th hour of TBI.
Results:
Higher myeloperoxidase activity levels in the TBI group (p < 0.001) were suppressed in the CA group (p < 0.05). Luminol 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). When compared to the elevated histological 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, p < 0.01; respectively) was not evident in the CA group.
Conclusion:
CA has shown neuroprotective effects by limiting neutrophil recruitment, suppressing reactive oxygen species, reducing histological damage, and acute hippocampal dysfunction.
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