Abstract

One of the most important medical and social problems of today is the search fornew pathogenetic areas of drug prevention and treatment of neurodegenerativediseases of the central nervous system. The pathogenesis of these processes has notbeen definitively studied, at the same time a number of scientific works testify to thesignificant role of the imbalance of the prooxidant- antioxidant system provoked by thehyperproduction of nitric oxide. Recent studies have also demonstrated the effect of nitricoxide on inhibiting GABA-ergic synaptic transmission. In addition, abnormal expressionof neuronal NO synthase has been found to be an early marker of Alzheimer’s disease andrelated cognitive impairment.Objective – to study the effect of carbacetam on the performance of nitric oxide andantioxidant enzymes in the cerebral cortex of rats under conditions of scopolamineinduced neurodegeneration.Materials and methods. The experiments were performed on nonlinear laboratory whitemale rats with scopolamine- induced neurodegeneration. The studies were performedin compliance with the Council of Europe Convention on the Protection of VertebrateAnimals. Carbacetam was administered intraperitoneally at a dose of 5 mg / kg (14 days).Antioxidant protection was assessed by the activity of superoxide dismutase (SOD) and catalase. The state of the NO system was determined by the content of stablemetabolites of nitric oxide – nitrite anions (NO2), and the activity of NO synthase.Results. In the group of rats with model pathology after 14 days of carbacetam therewas a tendency to decrease the content of NO2 and NO-synthase activity in the cerebralcortex in relation to untreated animals. At the same time, the activity of SOD and catalasedecreased in rats with neurodegeneration. After 14 days of carbacetam, catalase activityincreased and only a tendency to increase the activity of SOD was observed.Conclusion. Therefore, the obtained results allow judging the corrective effectof carbacetam on the nitric oxide system and the activation of antioxidant protection inthe cerebral cortex of rats with scopolamine- induced neurodegeneration.

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