Vitamin E protected cultured cortical neurons from oxidative stress-induced cell death through the activation of mitogen-activated protein kinase and phosphatidylinositol 3-kinase

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Abstract

The role of vitamin E in the CNS has not been fully elucidated. In the present study, we found that pre-treatment with vitamin E analogs including αT (α-tocopherol), αT3 (α -tocotrienol), γT, and γT3 for 24 h prevented the cultured cortical neurons from cell death in oxidative stress stimulated by H2O2, while Trolox, a cell-permeable analog of αT, did not. The preventive effect of αT was dependent on de novo protein synthesis. Furthermore, we found that αT exposure induced the activation of both the MAP kinase (MAPK) and PI3 kinase (PI3K) pathways and that the αT-dependent survival effect was blocked by the inhibitors, U0126 (an MAPK pathway inhibitor) or LY294002 (a PI3K pathway inhibitor). Interestingly, the up-regulation of Bcl-2 (survival promoting molecule) was induced by αT application. The up-regulation of Bcl-2 did not occur in the presence of U0126 or LY294002, suggesting that αT-up-regulated Bcl-2 is mediated by these kinase pathways. These observations suggest that vitamin E analogs play an essential role in neuronal maintenance and survival in the CNS.

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