Ischemia reperfusion injuries can be threatening to end organ viability and can progress, with mortal and morbid outcomes. In particular, neural tissues are highly sensitive to hypoxia and reperfusion stress. This study aimed to determine the neuroprotective effects of rosuvastatin on spinal cord ischemia reperfusion injury. Forty male Sprague- Dawley rats were divided into four equal groups: group I (control), group II (sham with simple laparotomy), group III (ischemia-reperfusion), group IV (ischemia-reperfusion group with continuous rosuvastatin utilization), and group V (ischemia-reperfusion group with rosuvastatin-withdrawal after reperfusion). Spinal cord ischemia was induced by clamping the aorta below the left renal artery and above the aortic bifurcation. Reperfusion was provided after 72(nd) hours of ischemia. After reperfusion, blood samples and spinal cord tissue samples were taken from all the rats. Oxidative and antioxidant markers from both serum and tissue samples were evaluated, and tissues were examined histopathologically. There were no significant differences between the control and sham groups. A notable increase in oxidative markers was observed in group III compared to group I. In addition, a significant decrease in antioxidant markers was detected in group III. However, there was a marked preservation in the tissue and blood samples of groups IV and V compared to group III in terms of oxidative damage. Additionally, definitive prophylaxes were seen in the histopathological examination of the tissue samples in groups IV and V compared with group III. These significant findings show that rosuvastatin has a considerable protective effect on neural tissue against oxidative damage. Likewise, the early withdrawal of rosuvastatin has a clear neuroprotective effect similar to that of continuous therapy. Nevertheless, other systematic effects and beneficial neural effects of statins should be investigated in further clinical trials.