Regulation of Cu-Zn superoxide dismutase on SCN2A in SH-SY5Y cells as a potential therapy for temporal lobe epilepsy

Xiang,Jun; Jiang,Yugang

doi:10.3892/mmr.2013.1790

Regulation of Cu-Zn superoxide dismutase on SCN2A in SH-SY5Y cells as a potential therapy for temporal lobe epilepsy

Authors:
- Jun Xiang
- Yugang Jiang
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Affiliations: Department of Neurosurgery, Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, P.R. China
Published online on: November 11, 2013 https://doi.org/10.3892/mmr.2013.1790
Pages: 16-22
Copyright: © Xiang et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 3.0].

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Abstract

In order to evaluate SCN2A as a candidate gene for epileptic susceptibility and the use of a Cu-Zn superoxide dismutase (SOD) supplement as a potential therapy for epilepsy, SCN2A expression in the cortex and the correlation between SCN2A and Cu-Zn SOD in SH-SY5Y cells were examined. SCN2A expression and the concentration of Cu-Zn SOD in the cerebral cortexes of patients with primary and secondary temporal lobe epilepsy and normal brain cortex tissues were detected. By transfecting SH-SY5Y cells, the expression of SCN2A and the concentration of Cu-Zn SOD was analyzed and the single-cell patch clamp technique was employed in order to investigate the changes in sodium ion levels following SCN2A knockdown. SCN2A level restoration was also investigated with a Cu-Zn SOD supplement using an expression study and evaluated the changes in sodium ion levels following SCN2A knockdown. SCN2A expression and Cu-Zn SOD concentration decreased in the epileptic cerebral cortex. Following SCN2A knockdown, the concentration of Cu-Zn SOD declined and the si-SCN2A vector group showed a repeated discharge. Furthermore, the Cu-Zn SOD concentration was capable of restoring the expression of SCN2A following SCN2A knockdown in SH-SY5Y cells and the overexpression of Cu-Zn SOD prevented the repeated discharge caused by si-SCN2A. The results indicated that there is a low expression of SCN2A and Cu-Zn SOD in the epileptic cerebral cortex and provided novel insights into potential therapies for temporal lobe epilepsy.

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