title: [The influence of insulin growth factor-I on the apoptosis of cardiomyocytes subjected to ischemia and hypoxia].
abstract: OBJECTIVE
  To investigate the influence of insulin growth factor-I (IGF-I) on apoptosis of cardiomyocytes subjected to ischemia and hypoxia and its possible mechanism.
  
  
  METHODS
  Cardiomyocytes were cultured in vitro, and randomized into hypoxia group, treatment group (T, the cells were treated with IGF-1 before subjected to hypoxia and ischemia) and control group (C, normal cardiomyocytes as controls). Changes in the OD value of cell apoptosis, mitochondrial membrane potential and relative amount of phospho-Akt protein were observed at different time-points by ELISA, laser scanning with TMRE staining and Western blot, respectively.
  
  
  RESULTS
  The OD value of cell apoptosis in control group was 0.18 +/- 0.03, while that in hypoxia group was gradually increased to 0.33 +/- 0.05, 0.61 +/- 0.06, 1.17 +/- 0.08, 2.25 +/- 0.11, respectively at 1, 3, 6, 12 post-hypoxia hours (PHH), showing an increasing tendency (P < 0.01). The OD values of cell apoptosis in T group were 0.26 +/- 0.04, 0.49 +/- 0.05, 0.84 +/- 0.06, 1.63 +/- 0.09, respectively, which were obviously lower than those in hypoxia group (P < 0.05 or P < 0.01). The mitochondrial membrane potential (Dymt) values in hypoxia group at 6 and 12 PHH were 18.7 +/- 5.1 and 6.3 +/- 1.9, respectively, which were obviously lower than that in control group (40.2 +/- 10.1, P < 0.01). The DYmt in T group at 6 and 12 PHH were 28.8 +/- 6.2, 12.5 +/- 3.1, respectively, which were obviously higher compared with those in hypoxia group (P < 0.05). The amount of phospho-Akt protein was increased by IGF-I administration.
  
  
  CONCLUSIONS
  IGF-I exhibits an anti-apoptotic effect on cardiomyocytes subjected to ischemia and hypoxia, and this may be related to the activation of PI3K/Akt signal pathway and stabilization of mitochondrial membrane potential.
authors.affiliation: Institute of Burn Research, Southwest Hospital, State Key Laboratory of Trauma, Burns and Combined Injury, Third Military Medical University, Chongqing 400038, PR China.
authors.forename: Hua-Pei
authors.initials: HP
authors.lastname: Song
authors.forename: Hong
authors.initials: H
authors.lastname: Yan
authors.forename: Dong-Xia
authors.initials: DX
authors.lastname: Zhang
authors.forename: Zhi-Gang
authors.initials: ZG
authors.lastname: Chu
authors.forename: Qiong
authors.initials: Q
authors.lastname: Zhang
authors.forename: Yue-Sheng
authors.initials: YS
authors.lastname: Huang
mesh_terms: D000818:Animals; D017209:Apoptosis; D015687:Cell Hypoxia; D002478:Cells, Cultured; D000860:Hypoxia / Q000378:metabolism*; D007334:Insulin-Like Growth Factor I / Q000494:pharmacology*; D007511:Ischemia / Q000378:metabolism*; D053078:Membrane Potential, Mitochondrial; D032383:Myocytes, Cardiac / Q000166:cytology*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D007334:Insulin-Like Growth Factor I; D051057:Proto-Oncogene Proteins c-akt