title: Expression of SOCSs and TLRs in the hippocampus of pentylenetetrazole kindling model.
abstract: BACKGROUND
  Epilepsy is one of the most common neurological disorders, and approximately one-third of patients with epilepsy are resistant to anti-epileptic drugs (AEDs). Recent emerging evidence has demonstrated the roles of innate immunity and the associated inflammatory processes in epilepsy. Toll-like receptors (TLRs) are a type of pattern-recognition receptor that promote innate immune defense. The SOCS proteins as negative-feedback regulators in cytokine signaling are involved in the regulation of TLR-mediated immune responses. However, few studies investigating the role of TLRs and SOCSs in epilepsy have been reported.
  
  
  METHODS
  To explore the role of innate immunity in the mechanism of epilepsy, the pentylenetetrazole (PTZ) kindling rat model was established using intraperitoneal injection of PTZ. The expression levels of TLR2, TLR4, and STAT molecules in rat hippocampi were analyzed using qRT-PCR and western blotting techniques. The expression levels of SOCS-1 and SOCS-3 in rat hippocampi were analyzed using qRT-PCR.
  
  
  RESULTS
  Our data demonstrated that both the mRNA and protein expression of TLR2 and TLR4 were significantly upregulated in the rat hippocampus with PTZ injection, which was accompanied by an inhibition of SOCS-1 and SOCS-3 and an upregulation of STAT3.
  
  
  CONCLUSIONS
  Our study suggested that SOCSs and TLRs contribute to the development of epilepsy which may lead to therapeutic interventions that limit epileptogenesis.
authors.forename: Ming-Yu
authors.initials: MY
authors.lastname: Song
authors.forename: Fa-Fa
authors.initials: FF
authors.lastname: Tian
authors.forename: Hao
authors.initials: H
authors.lastname: Liu
authors.forename: Yu-Zhong
authors.initials: YZ
authors.lastname: Wang
authors.forename: Jing
authors.initials: J
authors.lastname: Dang
authors.forename: Wen-Jiao
authors.initials: WJ
authors.lastname: Huang
authors.forename: Dong-Xue
authors.initials: DX
authors.lastname: Ding
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D015536:Down-Regulation / Q000187:drug effects / Q000235:genetics; D004827:Epilepsy / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D006624:Hippocampus / Q000187:drug effects* / Q000378:metabolism*; D053583:Interleukin-1beta / Q000378:metabolism; D007696:Kindling, Neurologic; D008297:Male; D010433:Pentylenetetrazole; D051381:Rats; D017207:Rats, Sprague-Dawley; D050791:STAT Transcription Factors / Q000378:metabolism; D050826:Suppressor of Cytokine Signaling Proteins / Q000235:genetics / Q000378:metabolism*; D051193:Toll-Like Receptors / Q000235:genetics / Q000378:metabolism*; D015854:Up-Regulation / Q000187:drug effects / Q000235:genetics
chemical_list: D053583:Interleukin-1beta; D050791:STAT Transcription Factors; D050826:Suppressor of Cytokine Signaling Proteins; D051193:Toll-Like Receptors; D010433:Pentylenetetrazole