The condition of rat periodontal tissues and correction by Cocarnit’ pathological changes were studied in the model of alcoholic neuropathy. The experiments were performed on 38 white nonlinear rats of both sexes weighing 180 – 220 g. Alcoholization of rats was carried out according to the following scheme: animals for 72 days were administered ethanol of various concentrations using a probe 1–24 days – 11.8%; 25–48 – 23.6%; 49–72 days – 37%. After confirmation of the development of polyneuropathy on the 72nd day of the experiment, was administered Cocarnit (World Medicine) intramuscularly for 9 days at a rate of 1 mg / kg dissolved in 0.5% lidocaine hydrochloride. In soft periodontal tissues of rats, the content of free fucose, glycosaminoglycans, total proteolytic activity, total antitryptic activity, content of TBA-active products, content of oxidatively modified proteins and catalase activity were determined. It was found that the alcoholization of rats caused an increase in the periodontal tissues of animals the content of TBA-active products, oxidatively modified proteins and catalase activity, which indicates the activation of free radical processes and the development of carbonyl oxidative stress. At the same time, the total proteolytic activity in periodontal tissues decreased against the background of reduced activity of proteinase inhibitors, which disrupted the remodeling of the extracellular matrix of connective tissue. Under these conditions, increased depolymerization of fucoproteins and proteoglycans of periodontal connective tissue was observed, as evidenced by the increase in the content of free fucose and glycosaminoglycans. It is substantiated that the introduction of Cocarnit in animals with simulated alcoholic neuropathy prevents depolymerization of biopolymers of the extracellular matrix of periodontal connective tissue and inhibits the development of carbonyl-oxidative stress.
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