Influence of ademol on the level of tumor necrosis factor α in the brain of rats with model of traumatic brain injury
Keywords:traumatic brain injury, tumor necrosis factor alpha, inflammation
Background. Identifying biomarkers of inflammation in traumatic brain injury (TBI) can be a valuable factual complement to improving the quality of prediction for brain injury outcomes. One such marker may be tumor necrosis factor alpha (TNF-α), which belongs to the group of proinflammatory cytokines. The purpose was to evaluate the effect of ademol compared with amantadine sulfate on TNF-α level in the brain of TBI rats. Materials and methods. The experiments were performed on male rats. An experimental model of severe TBI was created using a pneumatic gun. The therapeutic effect of ademol in TBI was evaluated at a dose of 2 mg/kg intravenously twice a day for 8 days. As the drug for the control group, 0.9% NaCl was used at a dose of 2 ml/kg, and as the comparison drug — amantadine sulfate at a dose of 5 mg/kg. The level of TNF-α was used to determine the efficacy of the investigated drugs. Results. A comparative analysis of the efficacy of ademol and amantadine sulfate on day 8 of observation showed that in the group of animals treated with ademol, the content of TNF-α in brain tissues has reduced by 57.3 % (p < 0.05) compared to the control pathology group, its median was 0.804 ng/g dry tissue (95% confidence interval 0.732–0.844). By the anti-inflammatory effect, amantadine sulfate was significantly inferior to ademol: so, in the group of rats treated with amantadine sulfate, the level of TNF-α in brain tissues was lower by 43.5 % (p < 0.05) compared to the control pathology group, its median was 1.02 ng/g dry tissue (95% interval 1.00–1.11). Conclusions. Experimental modeling of traumatic brain injury in rats was accompanied by the induction of an inflammatory response in brain tissues. One of the pathogenetic mechanisms of brain protective action in TBI is the ability of ademol to inhibit the development of an inflammatory response in the tissues of traumatically damaged brain by reducing TNF-α level (p < 0.05).
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