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Georgian Med News ; (318): 143-146, 2021 Sep.
Article in English | MEDLINE | ID: mdl-34628396

ABSTRACT

THE AIM OF THE STUDY: To determine the effect of Ademol on the deoxyribonucleic acid (DNA) fragmentation of the cerebral cortex cells (apoptosis) of rats with traumatic brain injury (TBI). MATERIALS AND METHODS: An experimental model of severe trauma was created in male rats using an air pistol. The therapeutic effect of Ademol in TBI was evaluated at a dose of 2 mg/kg intravenously at intervals of 2 t/d for 8 days. As a drug for the control group we used 0.9% NaCl at a dose of 2 ml/kg, and as a comparison drug - amantadine sulfate at a dose of 5 mg/kg. On day 8 after TBI and decapitation of animals, the parts of the cerebral cortex were taken to assess further DNA fragmentation in cells by the flow cytometry method. RESULTS AND CONCLUSIONS: The post-traumatic period of model TBI in rats is accompanied by a probable increase in the level of DNA fragmentation in the nucleus of cerebral cortex cells on the 8th day of the experiment. By the antiapoptotic effect in conditions of post-traumatic brain injury, Ademol solution therapy was significantly better than the infusion of 0.9% NaCl and amantadine sulfate at an average of 46.2 and 27.2%, respectively (p<0.05).


Subject(s)
Brain Injuries, Traumatic , Brain Injuries , Animals , Benzothiadiazines , Brain Injuries/drug therapy , Brain Injuries, Traumatic/drug therapy , Cerebral Cortex , DNA Fragmentation , Male , Rats , Rats, Sprague-Dawley
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