Abstract
Resume. Under the conditions of an experimental study of normoglycemic animals and the creation of aloxan sugar diabetes (ASD) as a premorbital background, iatrogenic damage to the lower alveolar nerve by filling materials based on resorcinol-formalin and epoxy resin causes destructive - degenerative changes, as evidenced by an increase in neuromarker titers NSE and S100 protein. After a 30-day therapy with a drug based on amantadine hydrochloride at a dose of 10 mg / kg, both indicators in both study groups significantly decreased. The titers of NSE and S100 protein in the group with ASD in both subgroups were 1.94 times, and 1.87 times less, which indicates the effectiveness of its use in this pathology, but compared with the group of normoglycemic animals, these indicators were 1.1 times and 1.72 times less, which occurred against the background of a parallel decrease in S 100 protein titers by 1.99 and 2.04 times, which indicates the presence of neuroprotective activity in this drug. This, in turn, is conducive to its further clinical research and the involvement of a drug based on amantadine hydrochloride in the main protocol for the treatment of patients with diabetes. Key words: iatrogenic compression-toxic lesion of the lower alveolar nerve, aloxan sugar diabetes, neuron-specific enolase, S 100 protein, amantadne hydrochloride, neuroprotection.
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