Neuroprotective Efficiency of Cyclosporine After Traumatic Brain Injury in Rats

Özet

AIM: To evaluate the possible neuroprotective effects of systemic administration of cyclosporine (Cyclosporin A) after traumaticbrain injury in rats.MATERIAL and METHODS: The modified Feeney method was used as the trauma model in male Sprague Dawley rats. After thetrauma, 20 mg/kg of cyclosporine was administered to the one group of the rats (n=12) intraperitoneally. Twenty-four hours afterinjury, the subjects were sacrificed, and brain samples were removed. The level of brain edema was evaluated through the wet-dryweight 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 significantneuroprotective effects of cyclosporine.CONCLUSION: The results demonstrated that systemic administration of cyclosporine produces a statistically significant decreasein both the level of brain edema and lipid peroxidation ratio when compared with “no treatment”. Cyclosporine, which is regularlyused as an immunosuppressant agent, is also known to prevent opening of the mitochondrial permeability transition pore byunbinding mitochondrial matrix cyclophilin. Regulation of transition pore for mitochondrial permeability by cyclosporine implies thatmitochondrial dysfunction following traumatic brain injury is an important event in the progressive loss of neuronal tissue.