Background: According to the experiments, neutrophils and microglial cells are the first to attend the early phase of events in inflammatory response to SCI. Those pilot cells are seen in the first 12-24 hours and disappear about 3-5 days. The neutrophil accumulation and activation are steered by many cytokines such as TNF-α, IL-1 and IL-6. Neutrophils do accompany to the modulation of secondary injury mechanisms via neutrophil proteases and reactive oxygen molecules. When those processes are taken into account, depletion of neutrophils or depression of their functions may derive neuro-protection and neurological healing.
Purpose: To investigate the therapeutic and neuroprotective effects of Cyclosporin-A (CSA) on recovery processes using clinical and histopathological tests, which has not been used very frequently in clip compression spinal cord injury (SCI) models.
Material and Methods: Twenty-four Spraque-Dawley rats were divided into three groups: group 1 [Sham-control, n=8], group 2 [SCI+2 mL saline intramuscular (i.m.), n=8], group 3 [SCI+5 mg/kg CSA (i.p.) 1 h after SCI and for the following three days, n=8]. Rats were evaluated 1st, 3rd, 5th and 10th days after SCI, clinically by Drummond and Moore scale and under light microscopy and by TUNEL test; after scarification on 10th day.
Results: Clinical and histopathological results of treatment group were found significantly better than the results of the trauma group.
Conclusion: CSA can depress apoptosis and necrosis rates in a statistically significant manner and carry out the statistical difference in clinical results.