TO DETERMINE THE CYCLOSPORINE NEUROPROTECTIVE EFFICIENCY AFTER TRAUMATIC INJURY OF BRAIN IN RATS

Aim: To evaluate the possible neuroprotective effects of systemic administration of cyclosporin (cyclosporin A) after traumatic brain injury in rats. Materials And Methods: The modified Feeney method was used as a model of trauma in male Sprague Dawley rats. After the injury, 20 mg / kg of cyclosporin was administered intraperitoneally to a group of rats (n = 15). Twenty-four hours after injury, the individuals were sacrificed and brain samples were collected. The brain edema level was assessed by lipid peroxidation rate, wet dry weight method and histological evaluation by transmission electron microscopy. Results: The brain edema level and the rate of lipid peroxidation were significantly reduced in the rats receiving cyclosporin. Ultrastructural neuro-destruction was assessed, and comparison of the results between experimental groups revealed a significant neuroprotective effect of cyclosporine. Conclusion: The results showed that systemic administration of cyclosporine resulted in a statistically significant reduction in both the level of brain edema and the rate of lipid peroxidation compared to the "untreated" state. It is also known that cyclosporine, which is regularly used as an immunosuppressant, prevents the opening of the pores of mitochondrial permeability by separating cyclophilin from the mitochondrial matrix. The transition pores regulation for the permeability of mitochondria by cyclosporine suggests that mitochondrial dysfunction following traumatic brain injury is an important event in progressive loss of neuronal tissue. Keywords: cyclosporine, neuroprotection, transitional pores of mitochondrial permeability, traumatic brain injury, rat