الفهرس 
title : Therapeutic potential of endothelial progenitor cells in a rat model of epilepsy: Role of autophagy and evaluation of promising long non-coding RNAs markers
AbstractOnly 14 pages are availabe for public view
 |  | from | 109 |  |  |
| | | from | 109 | | |
Abstract
Epilepsy is a chronic brain disease caused by abnormal discharge of cerebral neurons and characterized by chronic cognitive and neural dysfunction. An epileptic seizure results from transient abnormal synchronization of neurons in the brain that disrupts normal patterns of neuronal communication. The present study highlighted, for the first time, the potential therapeutic effects of endothelial progenitor cells (EPCs) in a pentylenetetrazole (PTZ)-induced epilepsy rat model. The study also intended to discover the link between autophagy modulation and epileptogenesis. Furthermore, certain pertinent long non-coding RNAs (lncRNAs) were also targeted. Male Wistar albino rats,weighing 170 ± 30 g, were randomly divided into four experimental groups, of 15 rats each. group I (Normal control) consisted of rats which received the vehicle only. group II (PTZ group) comprised rats which were subjected to intraperitoneal injections of a subconvulsive dose of PTZ (35 mg/kg) 3 times/week with a total of 9 injections, where three consecutive generalized convulsions (score 5 on Racine{u2019}s scale) were achieved by this regimen. group III (EPCs group) comprised kindled rats which received a single intravenous dose of EPCs (2{u00D7}106 cells) injected in the rat tail vein, after recording the first generalized convulsion. group IV (VPA group) consisted of kindled rats which received valproic acid (VPA) orally (150 mg/kg), as a reference antiepileptic drug, 30 min before each PTZ injection. After each PTZ injection, all animals were watched for 30 min to determine the seizure severity score according to Racine{u2019}s scale. At the end of the experimental period, rats were sacrificed by decapitation under light anesthesia 24 h after neurobehavioral assessment via performing Y-maze and open field (OFT) tests. Blood collected into heparin containing tubes was centrifuged and aliquots of the separated plasma were used for determination of the brain damage markers: soluble calcium binding protein 100-B (S100-B), neurofilament heavy chain protein (NEFH), heat shock protein-70 (HSP-70) and ubiquitin carboxy terminal hydrolyase-L1 (UCH-L1)