The effect of melatonin on spinal cord after ischemia in rats.

Experimental animal model to assess ischemic spinal cord injury (SCI) following occlusion of the thoraco-abdominal aorta. In the present study, we aimed to investigate the role of melatonin on SCI induced by ischemia and following reperfusion. Animal Research Laboratory, Inonu University, Malatya, Turkey. We evaluated oxidative damage and caspase-3 activity. In total, 32 adult Wistar albino rats were divided into four groups: Group 1, control (n=8); Group 2 (n=8), those subjected to ischemia/reperfusion (IR) by clamping the thoraco-abdominal aorta; Group 3 (n=8), melatonin (50 mg kg(-1)) treated; and Group 4 (n=8), melatonin (50 mg kg(-1)) followed by ischemia. All animals were kept alive for 48 h, and then spinal cord samples were removed. We assayed oxidative damage by measuring malondialdehyde (MDA), apoptosis by measuring activated caspase-3 (using immunoblots) and intrinsic antioxidative capacity by measuring reduced glutathione (GSH) levels in the spinal cord. The results indicated a significant decrease in activity of caspase-3 in SCI animals after treatment with melatonin, as it significantly decreased the formation of MDA and decelerated the loss of GSH. This study suggested that melatonin could be an effective neuroprotective agent for treatment of SCI.