中文摘要：

目的了解胰岛素样生长因子Ⅰ（IGF-I）对缺血缺氧致心肌细胞凋亡的影响，探讨其调控机制。方法分离培养SD乳鼠的心肌细胞。于制备缺血缺氧心肌细胞模型（缺血缺氧组）前1h，用IGF—I（200μg／L）进行干预（干预组），以缺血缺氧组致伤前测定结果为正常对照（对照组）。观察不同时相点心肌细胞凋亡的吸光度（A）值、线粒体膜电位变化及磷酸化Akt蛋白表达变化。结果对照组心肌细胞凋亡A值为0．18±0．03；缺血缺氧后1、3、6、12h分别为0．33±0．05、0．614-0．06、1．17±0．08、2．25±0．11，与对照组比较，差异有统计学意义（P〈0．01）；干预组上述时相点的A值分别为0．26±0．04、0．49±0．05、0．84±0．06、1．63±0．09，与缺血缺氧组比较差异有统计学意义（P〈0．05或P〈0．01）。缺血缺氧6、12h，心肌细胞线粒体膜电位荧光强度较对照组40．2±10．1下降，分别为18．7±5．1、6．3±1．9（P〈0．01），干预组较缺血缺氧组相对增高，分别为28．8±6．2、12．5±3．1（P〈0．05）。与对照组比较，其余各组缺血缺氧后6h磷酸化Akt蛋白表达量增加。结论IGF-I对缺血缺氧心肌细胞具有抗凋亡作用，其机制可能与IGF-I激活磷脂酰肌醇3-激酶／Akt、增加磷酸化Akt表达、减少细胞色素c的释放有关。

英文摘要：

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 controis）. 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 antiapoptotic 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.