title: Fetal bovine serum suppresses apoptosis in the small intestine after total ischemia and reperfusion in mice.
abstract: OBJECTIVE
  Total ischemia/reperfusion (I/R) of the small intestine induces cellular apoptosis. In this study, the authors investigated the effects of fetal bovine serum (FBS) on apoptosis and related proapoptotic and antiapoptotic factors in the I/R-injured small intestine of mice.
  
  
  METHODS
  The mice underwent total I/R of the small intestine and were treated with oral gavages of normal saline or FBS for 3 days, concluding with total ischemia of the small intestine. Samples of the I/R-injured small intestine, representing various predefined time-points post-I/R (immediately before and after 1 hour of total ischemia and at 1, 6, and 24 hours after initiation of reperfusion), were subjected to terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining to study the cellular apoptosis, and Western blot analysis to measure expression of p53, bcl-2 and bax, with caspase-activity assay used to determine the activity of caspase 3.
  
  
  RESULTS
  For the saline-treated mice, increased cellular apoptosis, suppressed expression of p53 and bcl-2 (with decreased bcl-2 to bax ratio) and increased caspase-3 activity were found for the I/R-injured small intestine. By contrast, FBS treatment suppressed cellular apoptosis, producing up-regulation of p53 and bcl-2 (with increased bcl-2 to bax ratio to 5.4-fold of the saline-treated group) and inhibiting the activity of caspase 3 (P <.05).
  
  
  CONCLUSIONS
  The results of our study suggest that I/R-induced apoptosis of the mouse small intestine may be related to p53 and bcl-2 suppression (with decreased bcl-2 to bax ratio) and activation of caspase 3 and that such apoptosis seems to be suppressed by FBS treatment.
authors.affiliation: Department of Surgery, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan.
authors.forename: Wen-Tsung
authors.initials: WT
authors.lastname: Hung
authors.forename: Yun
authors.initials: Y
authors.lastname: Chen
authors.forename: Sheng-Hong
authors.initials: SH
authors.lastname: Tseng
authors.forename: Hsiao-Lun
authors.initials: HL
authors.lastname: Li
authors.forename: Chia-Kang
authors.initials: CK
authors.lastname: Chen
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D002352:Carrier Proteins / Q000378:metabolism; D053148:Caspase 3; D020169:Caspases / Q000378:metabolism; D002452:Cell Count; D005312:Fetal Blood / Q000378:metabolism*; D007421:Intestine, Small / Q000098:blood supply* / Q000473:pathology*; D007511:Ischemia / Q000473:pathology* / Q000503:physiopathology*; D051379:Mice; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D044967:Serum / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism; D015854:Up-Regulation; D051028:bcl-2-Associated X Protein; D051025:bcl-Associated Death Protein
chemical_list: C494820:Bad protein, mouse; C494827:Bax protein, mouse; D002352:Carrier Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D016159:Tumor Suppressor Protein p53; D051028:bcl-2-Associated X Protein; D051025:bcl-Associated Death Protein; C505409:Casp3 protein, mouse; D053148:Caspase 3; D020169:Caspases