title: Erythropoietin reduces epileptogenic processes following status epilepticus.
abstract: OBJECTIVE
  Erythropoietin (EPO) has neuron and astroglial protective effects via reduction of tissue-injuring molecules such as reactive oxygen species, glutamate, inflammatory cytokines, and other damaging molecules. Although EPO may constitute an effective therapeutic modality in cases of epileptic insult, no study has been performed on the effects of exogenous EPO on the chronic seizure formation. In this study, we attempted to investigate if EPO could modulate the altered microenvironment in the epileptic rat brain.
  
  
  METHODS
  Morphological changes in the hippocampi of rats subjected to lithium-pilocarpine-induced status epilepticus (SE) were examined with respect to neuronal loss, inflammation, blood-brain barrier (BBB) leakage, and cell genesis. Spontaneous recurrent seizures (SRSs) were investigated by long-term video-EEG monitoring.
  
  
  RESULTS
  EPO receptor (EPOR) was found to be increased in the hippocampus after SE. Administered EPO prevented, during the latent period following SE, BBB leakage, neuronal death, and microglia activation in the dentate hilus, CA1, and CA3, and inhibited the generation of ectopic granule cells in the hilus and new glia in CA1. Moreover, EPO reduced the risk of SRS development.
  
  
  CONCLUSIONS
  These findings suggest that EPO has a potential therapeutic role in the setting of acute epileptic insults.
authors.affiliation: Stroke & Stem Cell Laboratory in Clinical Research Institute, Stem Cell Research Center, Department of Neurology, Seoul National University Hospital, Seoul, South Korea.
authors.forename: Kon
authors.initials: K
authors.lastname: Chu
authors.forename: Keun-Hwa
authors.initials: KH
authors.lastname: Jung
authors.forename: Soon-Tae
authors.initials: ST
authors.lastname: Lee
authors.forename: Jin-Hee
authors.initials: JH
authors.lastname: Kim
authors.forename: Kyung-Muk
authors.initials: KM
authors.lastname: Kang
authors.forename: Hyun-Kyung
authors.initials: HK
authors.lastname: Kim
authors.forename: Jae-Sung
authors.initials: JS
authors.lastname: Lim
authors.forename: Hee-Kwon
authors.initials: HK
authors.lastname: Park
authors.forename: Manho
authors.initials: M
authors.lastname: Kim
authors.forename: Sang Kun
authors.initials: SK
authors.lastname: Lee
authors.forename: Jae-Kyu
authors.initials: JK
authors.lastname: Roh
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001921:Brain / Q000473:pathology; D001973:Bromodeoxyuridine / Q000378:metabolism; D039481:CD11b Antigen / Q000378:metabolism; D002199:Capillary Permeability / Q000187:drug effects / Q000502:physiology; D016923:Cell Death / Q000187:drug effects; D004195:Disease Models, Animal; D004569:Electroencephalography / Q000379:methods; D004921:Erythropoietin / Q000627:therapeutic use*; D019793:Fluorescein; D005786:Gene Expression Regulation / Q000187:drug effects; D018398:Homeodomain Proteins / Q000378:metabolism; D008297:Male; D009474:Neurons / Q000187:drug effects; D010751:Phosphopyruvate Hydratase / Q000378:metabolism; D010862:Pilocarpine; D051381:Rats; D017207:Rats, Sprague-Dawley; D011994:Recombinant Proteins; D018709:Statistics, Nonparametric; D013226:Status Epilepticus / Q000139:chemically induced / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology*; D025521:Tumor Suppressor Proteins / Q000378:metabolism; D000098551:Prospero-Related Homeobox 1 Protein
chemical_list: D039481:CD11b Antigen; D018398:Homeodomain Proteins; D011994:Recombinant Proteins; D025521:Tumor Suppressor Proteins; D000098551:Prospero-Related Homeobox 1 Protein; D010862:Pilocarpine; D004921:Erythropoietin; D010751:Phosphopyruvate Hydratase; D001973:Bromodeoxyuridine; D019793:Fluorescein