Proteomics of epilepsy induced by focal disorder of cortical development

Objective To explore the proteomics of epilepsy induced by focal disorder of cortical development (DCD) in revealing the molecular mechanisms of epilepsy caused by DCD and looking for the candidate targets and new therapeutic approaches in clinical practice. Methods Animal models of DCD were established and induced by liquid nitrogen in healthy Wistar newborn rats. Animal model of DCD were divided into epilepsy group and control group according to Racine classification. The proteomics maps of the frontal cortex were obtained in the epilepsy group and the control group by two-dimensional electrophoresis and both Coomassie brilliant blue G250 and silver dying. The proteomics profiles of frontal cortex were preliminary analyzed with PD Quest 7.3 analysis package. The differentially expressed protein spots were excised from gel and digested with trypsin under optimal conditions. The masses of tryptic-digested peptides were acquired with a Voyager DA-STR matrix assisted laser desorption ionization time of flight (MALDI-TOF) mass spectrometer. The acquired monoisotopic masses of analyzed proteins were matched in silico with theoretical peptide masses of human protein in the swiss-prot database with a mass tolerance of less than 50 ppm. Results One hundred and three proteins of differential expression were observed in the frontal cortex tissues of epilepsy associated with disorder of cortical development in rats, in which 64 were detected to be up-regulated and 39 were down-regulated. Finally, 12 proteins were identified as Lissencephaly-1 protein, synaptotagmin Ⅳ, Glial fibrillary acidic protein, HSP70, growth associated protein 43, neuronal enolase, tubulin beta chain, glutamine synthetase, neuron cytoplasmic protein, voltage-dependent anion channel proteins 1, pyruvate kinase and neurofilament light polypeptide. Conclusion These proteins may play pivotal roles in the pathogenic mechanisms of epilepsy caused by disorder of cortical development and may provide new therapeutic targets for refractory epilepsy in the future. Key words: Disorder of cortical development; Epilepsy; Proteomics