COCARNIT CORRECTION OF PATHOLOGICAL CHANGES IN SALIVARY GLANDS OF RATS IN CONDITIONS OF DIABETIC NEUROPATHY
DOI:
https://doi.org/10.11603/mcch.2410-681X.2022.i1.13035Keywords:
diabetic neuropathy, salivary glands, Cocarnit, oxidative stressAbstract
Introduction. One of the most common complications of diabetes is the development of diabetic polyneuropathy, the effects of which on the salivary glands have not been sufficiently studied. The search for pharmacological correction based on the elucidation of the pathogenesis of the development of pathological changes in the salivary glands in diabetic neuropathy remains relevant.
The aim of the study – to study the effect of streptozocin-induced diabetic neuropathy on the development of pathological changes in the salivary glands of rats, as well as substantiating the feasibility of using the drug Cocarnit under these conditions.
Research Methods. Diabetic polyneuropathy in rats was induced by a single injection of sreptozocin (Streptozocin, Sigma, USA) at a dose of 65 mg/kg. The development of neuropathy was recorded with analgesimeter according to the Randall-Selitto method. Cocarnit (World Medicine) (1 mg/kg) was administered intramuscularly to rats for 9 days to correct the changes. In the homogenate of the mandibular salivary glands of rats, we determined the activity of α-amylase, catalase, level of medium weight molecules, TBA-active products and oxidatively modified proteins, total proteolytic and total antitryptic activity.
Results and Discussion. Experiments showed that the administration of streptozocin to animals resulted in an increase in the pain sensitivity threshold (PST) on all days of measurement compared to baseline. In rats injected with Cocarnit for 9 days, the PST was lower compared to the group of rats with diabetic polyneuropathy without correction and did not differ from the level of PST in the control. The development of diabetic neuropathy in the mandibular salivary glands of animals decreased amylalytic activity, increased antitryptic activity without changes in proteinase activity, and increased the content of TBA-active products compared to these indicators in control animals. Cocarnit administration for 9 days in diabetic neuropathy resulted in increased amylase activity, normalization of total antitryptic activity, and inhibition of lipid peroxidation in rat salivary glands compared to the uncorrected neuropathy model.
Conclusions. Cocarnit administration restored pain sensitivity to control values. Cocarnit normalized the suppressed protein-synthetic function of the salivary glands of rats in diabetic neuropathy and inhibited the development of oxidative stress.
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