Paralysis is one of the most common clinical manifestations of traumatic and non-traumatic complications that occur in the spinal cord tissue. Increased production of reactive oxygen species, decreased tis- sue antioxidant capacity, and consequently, oxidative stress would in- duce ischemia-reperfusion injury. The present study aims to investigate whether Trimetazidine, an anti-ischemic drug, may protect against the deleterious effects of spinal cord ischemia-reperfusion injury. Twen- ty-four Wistar rats were randomly divided into 4 groups: Sham (un- der exploratory abdominal surgery stress), TMZ (Trimetazidine drug only), IR (under abdominal aortic clamping surgery), and IR+TMZ (Trimetazidine treatment followed by aortic clamping surgery). To in- duce ischemia-reperfusion, the abdominal aortic was closed under the renal artery for 40 min. Posterior motor function was evaluated by the Tarlov grading system at 4, 6, 12, 24, 48, 60 hours after injury. Also, oxidative stress parameters including malondialdehyde (lipid perox- idation index) and antioxidant capacity with iron reduction (FRAP) were measured. The neural function of the IR + TMZ group was sig- nificantly increased at all times compared to the IR group (p <0.05). IR + TMZ group at 4and 6 hours after surgery was significantly different from sham group and TMZ group but in the following times, no sig- nificant difference was observed. Malondialdehyde levels in the spinal cord tissue were significantly increased in the IR group compared to the TMZ group (p <0.01) and IR + TMZ group as well as Sham group (p <0.05). The antioxidant capacity of the TMZ group was significant- ly higher than the Sham group and IR + TMZ group (p <0.05) and (p <0.01) respectively. The results of this study indicate that Trimetazi- dine can be effective in reducing spinal cord tissue injury by reducing the production of free radicals due to oxidative stress in spinal cord ischemia-reperfusion injury.

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