Ischemic heart disease (IHD) is the primary cause of death because of aging population in the world, which is characterized by reduced blood or oxygen supply to the heart. This study was aimed to indicate the biological process of Insulin-like growth factor 1 (IGF-1) on the IHD, as well as the functional role. Cell viability was determined by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT). Apoptosis cells were performed by flow cytometry. Reactive oxygen species (ROS)

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... levels were determined with 2,7-dichlorofluorescein diacetate (DCFH-DA) by flow cytometry. Western blot was used to analyze the protein expression of cytochrome C, B-cell lym-phoma-2 (Bcl-2), Phosphatidylinositol 3-kinase (PI3K)/AKT signaling after treatment with IGF-1 or IGF-1 receptor (IGF-1R) inhibitor. A model of ischemic and starved model was successfully induced in cardiac myoblast H9c2 cell line. An appropriate concentration of IGF-1 (50 ng/ml) was screened in ischemic H9c2 cells. Administration of IGF-1 statistically increased the cell viability (P < 0.05) compared to the control group, but decreased the cell apoptosis and ROS (P < 0.05). These effects were reversed by IGF-1R inhibitor. Besides, we demonstrated IGF-1 dramatically decreased cytochrome C release (P < 0.05) and up-regulated the Bcl-2 protein expression (P < 0.05), with p-AKT 308, p-AKT473, pERK , and p-S6 protein expression was increased (P < 0.05). Our studies indicate IGF-1 could promote cell viability, and inhibit cell apoptosis and ROS level by regulating PI3K/AKT signaling pathway.