Neuroprotective Effect of Vitamin E in a KainateInduced Rat Model of Temporal Lobe Epilepsy

• Published in: Neurophysiology (New York) Vol. 46; no. 2; pp. 126 - 133
• Main Authors: Kiasalari, Z., Khalili, M., Roghani, M.
• Format: Journal Article
• Language: English
• Published: Boston Springer US 01-04-2014; Springer Nature B.V
• Subjects: Biomedical and Life Sciences; Biomedicine; Epilepsy; Neurobiology; Neurosciences; Oxidative stress; Rodents; Vitamin E; temporal lobe epilepsy; mossy fiber sprouting; hippocampus; kainate; oxidative stress; vitamin E
• ISSN: 0090-2977; 1573-9007
• DOI: 10.1007/s11062-014-9418-5

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.