2014•Xiandai shengwu yixue jinzhanRequires access

Research on the Effects and Mechanisms of Melatonin on the Secondary brain Damage and Neurobehavioral Dysfunction after Experimental Subarachnoid Hemorrhage

WU Ling-yu

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Abstract

Objective: To investigate the effects and mechanisms of melatonin on the secondary brain damage and neurobehavioral dysfunction after experimental subarachnoid hemorrhage(SAH). Methods: 80 adult SD rats were divided into four groups: control group(n=20), SAH group(n=20), SAH+vehicle group(n=20), and SAH+melatonin group(n=20). The rat SAH model was induced by injection of 0.3 ml fresh arterial, nonheparinized blood into the prechiasmatic cistern in 20 s. In SAH+melatonin group, melatonin was administered i.p. at 150 mg/kg at 0, 12, 24 and 36 hr after the induction of SAH. Part of rats in each group were killed on 48 hr after SAH.The brain sample was removed and keeped in 10% formalin solution.Cognitive and memory changes were investigated in the Morris water maze at 48 hr after the induction of SAH with the rest of rats in each group. Results: The behavior and activity scores, escape latency and swimming distance in Morris water maze task, apoptosis and necrosis percentage of neurons of SAH rats were all significantly higher than those of the contol rats(P0.01), while the above index of SAH+melatonin group were significantly lower than those of the SAH+vehicle rats(P0.05), but no significant difference was found in the above index between SAH and SAH+vehicle rats(P0.05). Conclusion: Melatonin may improve the neurobehavioral dysfunction after SAH through decreasing the apoptosis and necrosis of neurons.

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Objective: To investigate the effects and mechanisms of melatonin on the secondary brain damage and neurobehavioral dysfunction after experimental subarachnoid hemorrhage(SAH). Methods: 80 adult SD rats were divided into four groups: control group(n=20), SAH group(n=20), SAH+vehicle group(n=20), and SAH+melatonin group(n=20). The rat SAH model was induced by injection of 0.3 ml fresh arterial, nonheparinized blood into the prechiasmatic cistern in 20 s. In SAH+melatonin group, melatonin was administered i.p. at 150 mg/kg at 0, 12, 24 and 36 hr after the induction of SAH. Part of rats in each group were killed on 48 hr after SAH.The brain sample was removed and keeped in 10% formalin solution.Cognitive and memory changes were investigated in the Morris water maze at 48 hr after the induction of SAH with the rest of rats in each group. Results: The behavior and activity scores, escape latency and swimming distance in Morris water maze task, apoptosis and necrosis percentage of neurons of SAH rats were all significantly higher than those of the contol rats(P0.01), while the above index of SAH+melatonin group were significantly lower than those of the SAH+vehicle rats(P0.05), but no significant difference was found in the above index between SAH and SAH+vehicle rats(P0.05). Conclusion: Melatonin may improve the neurobehavioral dysfunction after SAH through decreasing the apoptosis and necrosis of neurons.

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Available abstract

Objective: To investigate the effects and mechanisms of melatonin on the secondary brain damage and neurobehavioral dysfunction after experimental subarachnoid hemorrhage(SAH). Methods: 80 adult SD rats were divided into four groups: control group(n=20), SAH group(n=20), SAH+vehicle group(n=20), and SAH+melatonin group(n=20). The rat SAH model was induced by injection of 0.3 ml fresh arterial, nonheparinized blood into the prechiasmatic cistern in 20 s. In SAH+melatonin group, melatonin was administered i.p. at 150 mg/kg at 0, 12, 24 and 36 hr after the induction of SAH. Part of rats in each group were killed on 48 hr after SAH.The brain sample was removed and keeped in 10% formalin solution.Cognitive and memory changes were investigated in the Morris water maze at 48 hr after the induction of SAH with the rest of rats in each group. Results: The behavior and activity scores, escape latency and swimming distance in Morris water maze task, apoptosis and necrosis percentage of neurons of SAH rats were all significantly higher than those of the contol rats(P0.01), while the above index of SAH+melatonin group were significantly lower than those of the SAH+vehicle rats(P0.05), but no significant difference was found in the above index between SAH and SAH+vehicle rats(P0.05). Conclusion: Melatonin may improve the neurobehavioral dysfunction after SAH through decreasing the apoptosis and necrosis of neurons.

Key concepts: Melatonin, Subarachnoid hemorrhage, Medicine, Morris water navigation task, Anesthesia, Neuronal damage, Apoptosis, Brain damage

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