Fare Kafa Travması Modelinde Brimonidin Tartaratın Nöroprotektif Etkilerinin İncelenmesi
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Secondary brain injury resulting from head injury is usually related to cellular and molecular damage from the onset of the trauma to hours or days following the trauma. Brimonidine tartrate is a selective alpha-2 receptor agonist. There is no study showing the effect of Brimonidine tartrate, which is used in the treatment of glaucoma and known to have neuroprotective effects on retinal ganglion cells, on neuroinflammation in traumatic brain injury. In the study, a total of 21 male Swiss albino mice were divided into 3 groups and closed head trauma was created with a weight dropping model. The mice were sacrificed 24 hours after the trauma. After sacrifice, the brain tissues were examined by hemotoxylin & eosin stain and immunohistochemistry. NeuN positive cell count decreased significantly in the trauma group compared to the sham group (p = 0.0015). When the group that was applied brimonidine after trauma was compared with the group that was applied only to trauma, an increase was observed in the cells labeled with NeuN (p = 0.13). In the CD163 antibody labeling, 46.6% of the cells in the sham group, 65.1% in the trauma group, and 56.8% in the trauma + brimonidine group were marked positive with CD163 antibody. A statistically significant increase was found in the group that underwent trauma when the sham group was compared with the trauma group in marking with MHC2 antibody (p = 0.03). When trauma and trauma + brimonidine applied groups are compared; There was a decrease in the trauma + brimonidine group (p = 0.09). When the trauma and trauma + brimonidine groups were compared in the labeling with BDNF antibody, it was seen that the BDNF level increased in the trauma + brimonidine group, but this increase was not statistically significant (p = 0.19). Finally, in the brimonidine applied group absence of dense cell infiltration and edema in the parenchyma in the form of moth-eaten indicates it’s anti-inflammatory effect. Brimonidine has been shown to suppress neuroinflammation and microglial activation in a mouse head injury model. Brimonidine does not make a statistically significant difference in the early period, it is thought that this effect may occur cumulatively in the following days due to the nature of the secondary damage.