[The influence of insulin growth factor-I on the apoptosis of cardiomyocytes subjected to ischemia and hypoxia].

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.
Conclusion: 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.