Turkish Neurosurgery
Neuroprotective Efficiency of Cyclosporine A after Traumatic Brain Injury in Rats
Oktay Gurcan1, Merzuk Ozhan Uckun2, Ramazan Cengiz Celikmez3, Omer Faruk Turkoglu1, Hakan Eroglu4, Ethem Beskonaklı5, Levent Oner4, Yamac Taskın5
1Ankara Ataturk Education and Research Hospital, Neurosurgery, Ankara,
2Ankara Numune Education and Research Hospital, Neurosurgery, Ankara,
3Antalya Education and Research Hospital, Neurosurgery, Antalya,
4Hacettepe University Faculty of Pharmacy, Pharmaceutical Technology, Ankara,
5Private Practitioner of Neurosurgery, Ankara,
DOI: 10.5137/1019-5149.JTN.24303-18.2

Aim:The major focus of the study was to evaluate possible neuroprotective effects of systemic administration of cyclosporine (Cyclosporin A) after traumatic brain injury in rats.Material and Methods:The modified Feeney method was used as the trauma model in male Sprague Dawley rats. After the trauma, 20 mg/kg of cyclosporine was administered to the some of the rats intraperitoneally. Twenty-four hours after injury, the subjects were sacrificed, and brain samples were removed. The level of brain edema was evaluated through the wet-dry weight method, the lipid peroxidation ratio, and histological examination by transmission electron microscopy.Results:The level of brain edema and lipid peroxidation ratio significantly decreased in the rats that received cyclosporine. Ultrastructural neurodestruction was graded, and a comparison of the scores between the experimental groups revealed significant neuroprotective effects of cyclosporine.Conclusion:The results demonstrated that systemic administration of cyclosporine produces a statistically significant decrease both in the level of brain edema and in lipid peroxidation ratio in comparison with no treatment. Cyclosporine, which is regularly used as an immunosuppressant agent, is also known to prevent opening of the mitochondrial permeability transition pore by unbinding mitochondrial matrix cyclophilin. Regulation of transition pore for mitochondrial permeability by cyclosporine implies that mitochondrial dysfunction following traumatic brain injury is an important event in the progressive loss of neuronal tissue.

Corresponding author : Oktay Gurcan