title: [Effects of edaravone on glial fibrillary acidic protein and interleukin-lβ expression and neuronal apoptosis in juvenile rat hippocampus after status convulsion].
abstract: OBJECTIVE
  To study the effects of edaravone on glial fibrillary acidic protein (GFAP) and interleukin-1β (IL-lβ) expression and neuronal apoptosis in the juvenile rat hippocampus after status convulsion (SC).
  
  
  METHODS
  One hundred and ninety-five juvenile male Sprague-Dawley (SD) rats were randomly divided into 3 groups: normal saline control and SC with and without edaravone treatment. Each of the 3 groups was further subdivided into subgroups sacrificed at 4, 12, 24, 48 and 72 hrs after SC (n=15). The SC model was prepared using lithium-pilocarpine. The expression of GFAP and IL-lβ protein was detected with immunohistochemistry methods. The neuronal apoptosis was observed by TdT-mediated dUTP nick end labeling (TUNEL). The hippocampal GFAP mRNA expression was detected by RT-PCR.
  
  
  RESULTS
  The value of IOD of GFAP and IL-lβ positive cells measured by immunohistochemistry in the untreated SC group increased compared with the control group. Expression of GFAP and IL-lβ protein was significantly reduced in the edaravone treated SC group compared with the untreated SC group. RT-PCR showed the expression trend of GFAP mRNA was similar to that of protein. The TUNEL positive cells in the hippocampus CA1 in the untreated SC group increased significantly 12 hrs after SC and reached a peak at 48 hrs compared with the control group. The intervention with edaravone decreased significantly TUNEL positive cells between 12-48 hrs after SC, but the number of TUNEL positive cells in the intervention group remained significantly greater than in the control group.
  
  
  CONCLUSIONS
  The expression of GFAP and IL-lβ in the hippocampus increases after SC in rats. Edaravone may decrease the expression of GFAP and IL-1β and reduce the number of neuronal apoptosis. These results suggest that edaravone may have protective effects against brain damage caused by SC.
authors.affiliation: Department of Neurology, Sixth Hospital Affiliated to Zhejiang University of Traditional Chinese Medicine, Hangzhou 310014, China.
authors.forename: Hai-Ping
authors.initials: HP
authors.lastname: Wang
authors.forename: Xiao-Long
authors.initials: XL
authors.lastname: Deng
authors.forename: Guang-Qian
authors.initials: GQ
authors.lastname: Li
mesh_terms: D000818:Animals; D000983:Antipyrine / Q000031:analogs & derivatives* / Q000494:pharmacology; D017209:Apoptosis; D000077553:Edaravone; D016166:Free Radical Scavengers / Q000494:pharmacology*; D005904:Glial Fibrillary Acidic Protein / Q000032:analysis* / Q000235:genetics; D006624:Hippocampus / Q000378:metabolism*; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D053583:Interleukin-1beta / Q000032:analysis*; D008297:Male; D009474:Neurons / Q000473:pathology*; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D012640:Seizures / Q000378:metabolism* / Q000473:pathology
chemical_list: D016166:Free Radical Scavengers; D005904:Glial Fibrillary Acidic Protein; D053583:Interleukin-1beta; D012333:RNA, Messenger; D000077553:Edaravone; D000983:Antipyrine