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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,4值为0.1 8±0.03;缺血缺氧后1、3、6、12h分别为0.33±0.05、0.61±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。
Objective To investigate the effect of insulin-like growth factor I (IGF-I) on cardiomyocyte apoptosis induced by hypoxia and hypoxia, and to explore its regulatory mechanism. Methods The cardiomyocytes isolated from neonatal SD rats were isolated. One hour before the preparation of hypoxic-ischemic cardiomyocyte model (hypoxic-ischemic group), IGF-I (200μg / L) was used for intervention (intervention group). The pre-injury results of hypoxic- Control group). Absorbance (A), mitochondrial membrane potential and phosphorylated Akt protein expression in myocardial cells were observed at different time points. Results The control group showed cardiomyocyte apoptosis with a value of 4 ± 0.1 8 ± 0.03. The levels of myocardial cells in the control group were 0.33 ± 0.05, 0.61 ± 0.06, 1.17 ± 0.08 and 2.25 ± 0.11 at 1, 3, 6, and 12 hours after ischemia / hypoxia, respectively , The difference was statistically significant (P <0.01); the intervention group at the time point A value were 0.26 ± 0.04,0.49 ± 0.05,0.84 ± 0.06,1.63 ± 0.09, compared with the ischemia and hypoxia groups were statistically significant Significance (P <0.05 or P <0.01). Compared with the control group, the fluorescence intensity of mitochondrial membrane potential decreased at 6 and 12h of ischemia and hypoxia (18.7 ± 5.1, 6.3 ± 1.9, P <0.01) 28.8 ± 6.2, 12.5 ± 3.1 (P <0.05). Compared with the control group, the expression of phosphorylated Akt protein in the other groups increased 6 h after ischemia and hypoxia. Conclusion IGF-I may have anti-apoptotic effects on hypoxic-ischemic cardiomyocytes, and its mechanism may be related to the activation of phosphatidylinositol 3-kinase / Akt by IGF-I, the increase of phosphorylated Akt and the decrease of cytochrome c release.