Experimental spinal cord injury model to investigate the neuroprotective effects of Ederavone

SUMMARY Spinal trauma is an important cause of mortality and morbidity. More than half of the survivors are not capable of returning to their previous life style. This situation results a significant loss of human power in daily life. There are no medications except methylprednisolone which may improve the neurological function in patients with total spinal cord lesion. All those insults which can cause harm to the spinal cord such as trauma, hypoxia, hypoglycemia, epilepsy, toxins, neurodegenerative diseases, tumors show smilar characteristics of damage. Experimental work revealed that posttraumatic spinal cord injury is caused by a complex physiopathological process and the mechanisms are primary and secondary. The primary injury is the damage caused due to the mechanism and the severty of the initial trauma. The posttraumatic interval which endo up with huge amounts of axonal loss is called the secondary injury. The most important factor which initiates the degeneration after the spinal cord damage is lipid peroxidation Clinical observations showed that the posttraumatic spinal cord lesions enlarge due to the secondary insults. The underlying molecular and cellular mechanisms are not yet fully understood. Recent information discloses that free oxygen radical production and membrane lipid peroxidation have an important role in this issue. Edaravone is a good collector of hydroxy radicals and decreases the iron originated peroxidation injury. Besides its direct protective effect, edaravone triggers the release of IL-10 which has strong antiinflammatory and immunoregulatory characteristics. A correlation between spinal cord injury and IL-10 release has been reported. For these reasons, therapy with edaravone may trigger the release of IL-10 prevent this negative regulations. The neuroprotective effect of edaravone on experimental spinal cord injury has not been theroughly studied. Present study has been performed to investigate the neuroprotective effect of edaravone which has antioxidant and antiinflammatory effects on a experimental trauma model in rats. 24 Wistar-Albino rats ( 230-270 gr ) have been used in our study. Acute spinal cord trauma has been performed by weight drop method in general anesthesia. The animals are randomly gouped in three- control, trauma and therapy. The rats are sacrified one week after the experimental procedure and the ratio of spinal cord edema and the histopathology of traumatized spinal cord region are studied. When compared to the trauma group, the ratio for spinal cord edema and the damaged area of the spinal cord after histopathologic examination in therapy group were less. 59 Neurologic improvement has been observed in all groups after one week; but the improvement in therapy group was statistically better compared to the trauma group. In conclusions, all parameters revealed that edaravone has a neuroprotective effect after acute spinal cord trauma. Due to this results, more extensive research is needed for the confirmation of this fact in traumatic spinal cord injury and the future experimental results may create a better basis for clinical research.