Abstract:

Objective    To explore the pathogenesis mechanism and the potential therapeutic targets of intractable epilepsy through the technique of mitochondrial proteomics in pharmacoresistant epileptic models. Methods    Expression profiles of mitochondrial proteins in pharmacoresistant rats and non-pharmaco-resistant rats were compared and analyzed by using immobilized pH gradient, SDS-PAGE and matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF). Results    All 19 protein spots were differentially expressed when compared with non-pharmaco-resistant epileptic rats. 5 up-regulated proteins in pharmaco-resistant epileptic hippocampal mitochondria were glyceraldehydes-3-phosphate dehydrogenase, triosephosphate isomerase-1, voltage-dependent anion channel 1, aldose A, and tubulin beta 2. 14 down-regulated proteins in pharmacoresistant epileptic hippocampal mitochondria were aconitase, glutamate dehydrogenase 1, malate dehydrogenase, NADH dehydrogenase 1 alpha subcomplex 10, ATP synthase alpha subunit precursor, similar to pyruvate kinase isoenzyme, ATP binding cassette, subfamily B, member 10, phospholipase A2, serine proteinase inhibitor， serpin, heat shock protein 70, uncoupling protein, cofilin 1, aldehyde dehydrogenase, and voltage-dependent anion channel 2. Conclusion    Many mitochondrial proteins are differentially expressed, which are perhaps involved in the pathogenesis of intractable epilepsy.

Key words: Epilepsy; Mitochondria; Proteome; Pharmacoresistance