title: [Effects of nerve growth factor pretreatment on apoptosis of neurons and expression of Bcl-2, Bax protein in brain tissue following cerebral ischemia/reperfusion injury in gerbils].
abstract: OBJECTIVE
  To study the effect of nerve growth factor (NGF) pretreatment on apoptosis of neurons and the expression of Bcl-2 and Bax protein in cerebral cortex and hippocampus CA1 zone following global cerebral ischemia/reperfusion (I/R) injury in gerbils and to explore the mechanism of protection and the best time window of NGF pretreatment.
  
  
  METHODS
  Global cerebral I/R injury model was induced by occlusion of bilateral carotid arteries. NGF was injected into the lateral ventricle. Thirty gerbils were randomly divided into five groups, with six animals in each: sham operation group (A group), I/R injury group (B group), NGF pretreatment 12, 24 and 48 hours groups (C, D and E group). Gerbils in all groups were sacrificed after being subjected to 20 minutes of cerebral ischemia followed by 72 hours reperfusion, except A group. Neural apoptosis was identified by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL), and immunohistochemistry was used to detect the expression of Bcl-2 and Bax protein in cerebral cortex and hippocampus CA1 zone.
  
  
  RESULTS
  Compared with B group, the number of apoptotic neurons and the expression of Bax positive cells in NGF pretreatment groups were decreased significantly (all P<0.05), while the expression of Bcl-2 positive cells was increased significantly (all P<0.05). The apoptotic rate in cerebral cortex and hippocampus CA1 zone and expression rate of Bax protein positive cells were the lowest, but the expression rate of Bcl-2 protein positive cells was the highest at 48 hours.
  
  
  CONCLUSIONS
  NGF pretreatment can significantly decrease the neuronal apoptosis of the cerebral I/R injury in gerbils, and the best time window of NGF pretreatment is 48 hours. The mechanism of protection may be related to induction of Bcl-2 protein expression and inhibition of Bax protein expression by NGF pretreatment, thereby preventing neuronal apoptosis.
authors.affiliation: Intensive Care Unit, Affiliated Hospital of Guiyang Medical College, Guiyang 550004, Guizhou, China. tanyongxing24@163.com
authors.forename: Yong-xing
authors.initials: YX
authors.lastname: Tan
authors.forename: Di-fen
authors.initials: DF
authors.lastname: Wang
authors.forename: Xue-mei
authors.initials: XM
authors.lastname: Li
authors.forename: Xing-min
authors.initials: XM
authors.lastname: Liu
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D002545:Brain Ischemia / Q000378:metabolism / Q000473:pathology*; D004195:Disease Models, Animal; D005260:Female; D005849:Gerbillinae; D006624:Hippocampus / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D008297:Male; D020932:Nerve Growth Factor / Q000494:pharmacology*; D009474:Neurons / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D011897:Random Allocation; D015427:Reperfusion Injury / Q000378:metabolism / Q000473:pathology*; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; D020932:Nerve Growth Factor