Relevance. A key role in the pathogenesis of brain injury (BI) is played by destructive changes in the neural tissue of the brain, which consist in damage to neurons and glial cells. To date, various drugs are being intensively developed and studied, which are considered in the perspective of correction and restoration of the functional state of the brain. These substances include the neuroprotector carbacetam, an modulator of the GABA-benzodiazepine receptor complex, a derivative of the alkaloid β-carboline.
Objectie. To investigate the effect of carbacetam on neurodestruction processes in the paraventricular and supraoptic nuclei of the hypothalamus in experimental BI.
Material and methods. The study was carried out on 20 white non-native male rats weighing 200±10 g. To simulate the BI, rats were subjected to one stroke along the cranial vault with a free-fall load according to the V.N. Yelskyy and S.V. Ziablitsev method (2008). The energy of impact was 0.52 J, the lethality for the first 5 days after injury was 84%. In the control group (n=10) 1 ml of saline was injected intraperitoneally once daily for 10 days after injury. Animals of the experimental group (n=10) received intraperitoneally injections of carbacetam at a dose of 5 mg/kg in 1 ml of saline according to the same scheme. After the experiment was over, the animals were decapitated with the removal of the brain, from which histological preparations were made with a microtome after appropriate histological treatment. Some sections were stained with hematoxylin and eosin, others were immunohistochemically reacted with antibodies against neuronmarkers proteins NSE, S-100 and GFAP.
Results. Carbacetam influenced the decrease of degenerative processes in the nervous tissue of the paraventricular and supraoptic nuclei of the hypothalamus. Neurons of animals with BI that received carbacetam, were characterized by the restoration of normal morphological features in contrast to rats not receiving the drug. Immunohistochemical study of brain neuromarkers confirmed the restoration of the functions of neurons and astrocytes in the investigated parts of the rat's hypothalamus after the administration of carbacetam. There was a decrease in the expression level of glial markers GFAP and S-100, which illustrated the decrease in degenerative changes in the nervous tissue. While the expression level of the neuron marker NSE grew, this demonstrated the high metabolic activity of nerve cells. Changes in the expression of markers of neurons and glia indicated a restoration of normal neuronal activity under the action of carbacetam.
Conclusion. Further investigation of the effects of carbacetam seems promising in terms of the restoration of neuronal function at BI.
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