Expression And Functional Analysis Of Differential Protein On Hippocampus In Rats With Temporal Lobe Epilepsy Induced By Kainic Acid

Purpose and Background:We study the pathological changes and differentially expressedproteins of hippocampus in rats with temporal lobe epilepsy (TLE)induced by kainic acid (KA). then discuss the mechanism of braininjury after epilepsy, provide clues to elucidate the pathogenesis of TLE,and provide molecular targets for the development of new antiepilepticdrugs.Materials and Methods:（1）Experimental animals grouping and Model preparation: themale Wistar rats were randomly divided into normal control group (n=6,without any disposal), operation control group (n=10, injected with PBSin the right side of the amygdale) and temporal lobe epilepsy group (n=12,injected with KA in the right side of the amygdala).（2） Using light microscope to observe the hippocampalpathological changes of each group, and do the comparative analysis.（3） Using two-dimensional difference gel electrophoresis(2D-DIGE), DeCyder analysis software and matrix assisted laserdesorption ionization tandem time of flight mass spectrometry(MALDI-TOF/TOF-MS) to separate, analyse and identify the differentially expressed proteins of hippocampus tissue.Results:(1) The rats injected with KA showed partial seizures, and thenevolved into generalized seizures, similar to the behavior characteristicsof TLE in human.(2) Hippocampal damage of epileptic group was located at CA3areamainly, the hippocampus of the two control group had no obviouspathological changes.(3) We had identified10differentially expressed proteins. tubulinalpha-1B chain, glial fibrillary acidic protein (GFAP),dihydropyrimidinase-related protein2(DRP-2), calponin-3, annexin A3,Proteasome activator complex subunit1(PA28α), translationallycontrolled tumor protein (TCTP) and the unnamed protein product wereup-regulated. Ezrin and hippocalcin were down-regulated. AnnexinA3, PA28α, TCTP and hippocalcin were first reported in TLE.Conclusion:（1）We had further confirmed the hippocampal pathologicalchanges of TLE induced by KA.（2）We had studied the proteomics of hippocampus in rats withTLE induced by KA, and identified10differentially expressed proteins;There were8up-regulated proteins which showed that synaptic plasticity,glial cell proliferation, increased neuronal excitability, inflammationand immune response may participate in the occurrence and development of epilepsy; The other2down-regulated proteins confirmed that theabnormal cytoskeleton and calcium overload play an important role in thepathogenesis of TLE.（3）Annexin A3, PA28α, TCTP and hippocalcin were first foundto be related to TLE.（4）The identified differentially expressed proteins provided cluesto elucidate the pathogenesis of TLE and develop molecular targets ofnew antiepileptic drugs.