Protective effect of melatonin on experimental spinal cord ischemia

Abstract

Study design: Experimental animal model to assess ischemic spinal cord injury following occlusion of the thoraco-abdominal aorta. Objectives: To measure whether melatonin administered to rabbits before and after occlusion exerts an effect on the repair of ischemia-reperfusion (IR) injury. Setting: Medical Biology Laboratory, Inonu University, Malatya, Turkey Methods: Rabbits were divided into three IR treatment groups and one sham-operated (ShOp) control group. The three treatment groups had their infrarenal aorta temporarily occluded for 25 min, while the ShOp group had laparotomy without aortic occlusion. Melatonin was administered either 10 min before aortic occlusion or 10 min after the clamp was removed. Physiologic saline was administered to the control animals. After treatment, the animals were euthanized and lumbosacral spinal cord tissue was removed for the determination of relevant enzyme activities. Results: Malondialdehyde levels, indicating the extent of lipid peroxidation, were found to be significantly increased in the nonmelatonin treated (IR) group when compared to the ShOp group. Melatonin, whether given to pre-or post occlusion groups, suppressed malondialdehyde levels below that of the ShOp group. Catalase (CAT) and glutathione peroxidase (GSH-Px) enzyme activities were increased in the IR group compared to the ShOp group. Melatonin given preocclusion resulted in a significant decrease in both CAT and GSH-Px enzyme levels. The superoxide dismutase (SOD) enzyme activity was decreased in the ischemia-reperfusion treatment group. However, the melatonin treatment increased SOD enzyme activity to levels approximating that of the ShOp group. Conclusion: To our knowledge, this is the first study that shows the effects of melatonin administered both pre-and postischemia on induced oxidative damage to injured spinal cords. Our data also expands on reports that melatonin administration may significantly reduce the incidence of spinal cord injury following temporary aortic occlusion.

The effects of prophylactic zinc and melatonin application on experimental spinal cord ischemia–reperfusion injury in rabbits: experimental study

“…Data were analyzed with one-way ANOVA (group 1: control, group 2: I/R, group 3: I/R þ zinc, group 4: I/R þ mel, group 5: I/R þ zinc þ mel). *Po 0.05 compared to groups 1, [3][4][5] other hand, it is stated that melatonin treatment, affecting pro-oxidant enzyme activity, has a protective role against lipid peroxidation. 11 As similar results were obtained in our study, it is compatible with the mentioned study.…”

“…1,2 The neurological damage to the spinal cord due to ischemia-reperfusion (I/R) injury has an average incidence ranging from 3 to 33%. 1,2,3 Free radicals are reactive molecules that emerge in traumatic brain injury and in the pathology of cerebral ischemia and they also constitute the mechanism known as oxidative stress. 4 Melatonin, which is the main secretion product of the pineal gland, functions as a strong free radical scavenger and an antioxidant.…”

The effect of melatonin on spinal cord after ischemia in rats

“…4 In experimental animal models of SCI, melatonin has been found highly effective in reducing the level of lipid peroxidation following injury. 5 This effect may be due to the facts that melatonin is a powerful antioxidant, and it stimulates several antioxidants including: catalase, glutathione reductase, peroxidase and superoxide dismutase. Melatonin has been shown to be highly effective in reducing oxidative damage in the central nervous system; its efficacy derives from its ability to directly scavenge a number of free radicals and to function as an indirect antioxidant.…”

Effects of iloprost and piracetam in spinal cord ischemia–reperfusion injury in the rabbit

“…1,2 The incidence of neurological injury occurring as a result of ischemia/reperfusion (I/R) injury to the spinal cord ranges between 4 and 33%. [1][2][3] Various methods have been proposed to protect the spinal cord from this complication. 4,5 However, paraplegia seems to be a durable complication, 6 and the mechanism of this complication is not yet fully understood.…”