Abstract: Objective To investigate the effects of melatonin on oxidative stress and neuronal apoptosis in hippocampus of epileptic rats and the mechanism. Methods Seventy-two adult male Sprague-Dawley rats were equally divided into control group, model group, low dose group and high dose group. The model group was injected coriamyrtin 50 μg/kg in the lateral ventricle, while the low dose group and high dose group were injected melatonin 20 mg/kg and 60 mg/kg, respectively, 30 minutes before injection of coriamyrtin. The contents of malondialdehyde (MDA) and superoxide dismutase (SOD) were detected with ultraviolet spectrophotometer, the apoptosis was detected with TUNEL, and the ultrastructural changes of neurons and mitochondria in hippocampal CA3 region were observed with electron microscopy, after 60 minutes of epilepsy. Results The neurons and mitochondria in hippocampus were damaged, the number of apoptotic cells significantly increased (P<0.001), the content of SOD decreased (P<0.001), and the content of MDA increased (P<0.001) in the model group, compared with the control group. In the low dose group, the ultrastructural damage relieved, the number of apoptotic cells decreased (P<0.01), the content of SOD increased (P<0.05), and the content of MDA decreased (P<0.05); and for the high dose group, the ultrastructural damage relieved very much, the number of apoptotic cells decreased (P<0.001) and was not significantly different from the control group (P>0.05), SOD increased (P<0.001), and MDA decreased (P<0.001), compared with the model group. Conclusion Exogenous melatonin may significantly reduce neuronal apoptosis in rat hippocampal after epilepsy, and high dose is more effective, which may relate with resistance of oxidative stress, alleviate neuronal mitochondrial damage.

Key words: epilepsy, melatonin, oxidative stress, apoptosis, ultrastructure, rats