Neuroprotective effect of vitamin E in a kainate-induced rat model of temporal lobe epilepsy

Temporal lobe epilepsy (TLE) is known as the most common form of epilepsy in adults and as the type most resistant to treatment. Neuroprotective treatments are considered a promising therapy for preventing and treating TLE. We investigated the possible neuroprotective effect of vitamin E in an intrahippocampal kainate model of TLE in rats. Kainate injection caused a higher incidence rate of seizures; vitamin E pretreatment significantly attenuated this index. Intrahippocampal kainate also led to elevation of the malondialdehyde (MDA) and nitrite/nitrate levels and lowered superoxide dismutase (SOD) activity, while vitamin E significantly restored MDA and SOD indices. In addition, intrahippocampal kainate induced a significant degeneration of neurons in the CA1, CA3, and hilar regions of the hippocampus; vitamin E considerably attenuated these changes. Timm staining data demonstrated mossy fiber sprouting (MFS) in the dentate gyrus of kainate-lesioned rats, and vitamin E significantly lowered the MFS intensity. Our data suggest that vitamin E pretreatment is capable of attenuating seizures and inhibiting hippocampal neuronal loss and MFS in the kainate-induced model of TLE. A part of the beneficial vitamin E effect is due to its potential to mitigate oxidative stress.