title: [Neural apoptosis and apoptosis-related genes in intracerebral hemorrhage patients].
abstract: OBJECTIVE
  To observe the neural apoptosis and expression of apoptosis-related genes in brain in order to elucidate the regulation mechanism in the perihematomal region of intracerebral hemorrhage (ICH) patients.
  
  
  METHODS
  Specimens of perihematomal region in human brain were obtained from 29 patients undergoing surgical evacuation of an intracerebral hematoma. Specimens of brain tissue were collected from the corpses of 6 persons within 3 hours after the accidental death. Neural apoptosis was evaluated by terminal deoxynucleotidyl transferase-mediated deoxyuridine 5' triphosphate nick end labeling (TUNEL) method and immunohistochemistry was used to detect the expression of Bcl-2, Bax, P53, and caspase-3 genes.
  
  
  RESULTS
  The apoptosis rates of the ICH group was 4.10 +/- 0.28, significantly higher than that of the control group (0.57 +/- 0.43, P < 0.01). The expression rate of Bcl-2 the ICH group was 2.68 +/- 0.52, significantly higher than that of the control group (1.54 +/- 0.56, P < 0.01). The expression rate of Bax of the ICH group was 3.49 +/- 0.18, significantly higher than that of the control group (0.96 +/- 0.27, P < 0.01). The expression of P53 was 4.12 +/- 0.63, significantly higher than that of the control group (0.96 +/- 0.71, P < 0.01). The expression of caspase-3 of the ICH group was 3.50 +/- 0.25, significantly higher than that of the control group (0.74 +/- 0.73, P < 0.01). The expression levels of Bcl-2 and P53 were negatively correlated with the apoptosis rate (both P < 0.01), while the expression levels of Bax and caspase-3, and the Bax/Bcl-2 ratio were positively correlated with the apoptosis rate in perihematomal region of ICH patients (all P < 0.01).
  
  
  CONCLUSIONS
  Apoptosis is involved in the delayed brain injury after ICH in human and is the main factor of delayed neural death. Some of the genes take part in the regulation of neural apoptosis: Bax and caspase-3 hasten the apoptosis while Bcl-2 and P53 restrain it.
authors.affiliation: Department of Neurology, Second Clinical Academy of Fujian College of Traditional Chinese Medicine, Fuzhou, 350003, China.
authors.forename: Cheng-han
authors.initials: CH
authors.lastname: Wu
authors.forename: Xi-yan
authors.initials: XY
authors.lastname: Ding
authors.forename: Hai-yan
authors.initials: HY
authors.lastname: Wang
authors.forename: Xiao-bao
authors.initials: XB
authors.lastname: Ye
authors.forename: Sheng-yue
authors.initials: SY
authors.lastname: Huang
authors.forename: Ai-min
authors.initials: AM
authors.lastname: Huang
authors.forename: Hui-zhong
authors.initials: HZ
authors.lastname: Li
authors.forename: Song-ying
authors.initials: SY
authors.lastname: Wu
authors.forename: Ji
authors.initials: J
authors.lastname: Yu
authors.forename: Xiao-hua
authors.initials: XH
authors.lastname: Yan
mesh_terms: D000328:Adult; D000368:Aged; D017209:Apoptosis; D051017:Apoptosis Regulatory Proteins / Q000096:biosynthesis*; D053148:Caspase 3 / Q000096:biosynthesis; D005260:Female; D006406:Hematoma / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D020299:Intracranial Hemorrhage, Hypertensive / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009474:Neurons / Q000378:metabolism* / Q000473:pathology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis
chemical_list: D051017:Apoptosis Regulatory Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D016159:Tumor Suppressor Protein p53; D053148:Caspase 3