title: [Effects of scutellaria stem-leaf total flavonoids on cardiocyte apoptosis induced by hypoxia/reoxygenation].
abstract: OBJECTIVE
  To study the effect of Scutellaria baicalensis stem-leaf total flavonoids (SSTF) on cardiocyte apoptosis of neonatal rats induced by hypoxia/reoxygenation and its action of mechanism. METHODS Sixty one to two days old rats, male or female, were selected. Hypoxia/reoxygenation injured model was established in cultured cardiocytes of neonate rats. The cultured neonatal rat cardiocytes were divided into 5 groups, i.e., the normal control group, the hypoxia/reoxygenation injury group (as the model group, cultured cardiocytes were exposed to hypoxia 2 h and subsequently reoxygenated for 4 h), the hypoxia/reoxygenation injury plus 50 mg/L SSTF group (as the low dose SSTF group), the hypoxia/reoxygenation plus 100 mg/L SSTF group (as the middle dose SSTF group), and the hypoxia/reoxygenation plus 200 mg/L SSTF group (as the high dose SSTF group). The cell viability was detected by methyl thiazolyl tetrazolium (MTT) colorimetry. The apoptosis of cardiocytes was determined by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) and the apoptosis rate calculated. The Bcl-2 and Bax protein expressions were determined by immunohistochemistry.
  
  
  RESULTS
  Compared with the normal control group, the cell viability, Bcl-2 protein contents and Bcl-2/Bax decreased, the apoptosis rate and Bax protein contents increased in the model group (all P<0.01). Compared with the model group, the cell viability, Bcl-2 protein contents and Bcl-2/Bax increased, while the apoptosis rate and Bax protein contents decreased in each SSTF treated group (P<0.05, P<0.01). Compared with the low dose SSTF group, significant difference existed in each index of the high dose SSTF group (all P<0.05).
  
  
  CONCLUSIONS
  SSTF had protection on hypoxia/reoxygenation induced cardiocyte apoptosis. Its protective mechanism might be correlated with its up-regulation of the expression of Bcl-2 protein ahd down-regulation of the expression of Bax protein.
authors.affiliation: Department of Biochemistry, Chengde Medical College, Hebei 067000. zxh5055@sina.com
authors.forename: Xiao-hui
authors.initials: XH
authors.lastname: Zhou
authors.forename: Ming-yu
authors.initials: MY
authors.lastname: Gong
authors.forename: He-mei
authors.initials: HM
authors.lastname: Yang
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D015687:Cell Hypoxia / Q000187:drug effects; D002478:Cells, Cultured; D005260:Female; D005419:Flavonoids / Q000494:pharmacology*; D008297:Male; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000378:metabolism; D018547:Plant Stems / Q000737:chemistry; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D031363:Scutellaria / Q000737:chemistry; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: C494828:Bax protein, rat; D005419:Flavonoids; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein