title: Correlation of free radical level and apoptosis after intracerebral hemorrhage in rats.
abstract: OBJECTIVE
  To investigate the correlation of perihematomal free radical level and neuronal apoptosis following the intracerebral hemorrhage (ICH).
  
  
  METHODS
  Animals were randomly divided into 4 groups: sham operation group, model group, 1 mg/kg edaravone group, and 3 mg/kg edaravone group. Each group was then divided into seven subgroups, in which the rats were correspondingly killed at 6 h, 12 h, 24 h, 48 h, 72 h, 7 d or 14 d (n = 1 in each subgroup of the sham group, and n = 6 in each subgroup of the other 3 groups). By Horseley-Clarke technique, autoblood (80 microL) were administered into the left caudate putamen of SD rats in a double administration-withdrawal way. Rats in the sham group were needled in but not administered with autoblood. The ICH model was then evaluated by Bederson's scale. Around the hematoma, the levels of malonaldehyde (MDA) and hydroxyl radical were tested by spectrophotometer, and the process of apoptosis was tested by terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL) method.
  
  
  RESULTS
  (1) ICH significantly increased the levels of MDA and hydroxyl radicals. Significant differences in MDA and hydroxyl radical contents were observed among the four groups. (2) In the sham group, a small number of TUNEL-positive cells were found. In the other three groups, the TUNEL-positive cells were observed at 6 h, increased significantly at 24 h, and reached peak level at 3 d, then fell profoundly at 7 d, but remained detectable at 14 d. (3) The positive correlation existed between apoptosis and free radical level (r = 0.2003), and existed between apoptosis and MDA content (r = 0.6563) in the brain.
  
  
  CONCLUSIONS
  Post-hemorrhagic apoptosis was related to the production of free radicals, indicating that the elevated free radicals following the ICH could induce neuron and glial cell apoptosis.
authors.affiliation: The Changhai Hospital Affiliated to the Second Military Medical University, Shanghai, China.
authors.forename: Ning
authors.initials: N
authors.lastname: Han
authors.forename: Su-Ju
authors.initials: SJ
authors.lastname: Ding
authors.forename: Tao
authors.initials: T
authors.lastname: Wu
authors.forename: You-Li
authors.initials: YL
authors.lastname: Zhu
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D000983:Antipyrine / Q000031:analogs & derivatives* / Q000627:therapeutic use; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology*; D002543:Cerebral Hemorrhage / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D000077553:Edaravone; D016166:Free Radical Scavengers / Q000627:therapeutic use*; D017665:Hydroxyl Radical / Q000378:metabolism*; D020287:In Situ Nick-End Labeling / Q000379:methods; D016014:Linear Models; D008297:Male; D008315:Malondialdehyde; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors
chemical_list: D016166:Free Radical Scavengers; D017665:Hydroxyl Radical; D008315:Malondialdehyde; D000077553:Edaravone; D000983:Antipyrine