| Objective To investigate the regulatory role and mechanism of insulin-like growth factor 1 (IGF-1) mediated mitogen-activated protein kinase (MAPKs) signaling pathway in osteogenic differentiation of C3H10T1/2 cells. Methods C3H10T1/2 cells were cultured with different concentrations of IGF-1 (0, 5, 10, 20 ng/mL). ALP activity and calcium salt deposition were detected by alkaline phosphatase (ALP) and alizarin red (ARS) staining. mRNA expression levels of core binding factor α-1 (RUNX2), osteopontin (OPN) and osteocalcin (OCN) were detected by qRT-PCR, and phosphorylated expression levels of MAPK pathway proteins were detected by Western Blot. Logarithmic cells were divided into blank group, IGF-1 group, ERK pathway inhibitor (PD98059) group, PD+IGF-1 group, p38 pathway inhibitor (SB202192) group and SB+IGF-1 group. mRNA expression levels of osteogenic characteristic factor RUNX2, osteopontin (OPN) and osteocalcin (OCN) were detected by qRT-PCR. Results In different concentrations of IGF-1 groups, ALP color rendering was deepened, ALP activity was increased, the formation of calcium salt nodules was increased, mRNA expression levels of RUNX2, OPN and OCN were increased, and protein expressions of phosphorylated ERK, p38 and JNK were increased, with dose effect (P< 0.05). Compared with blank group, the mRNA expression levels of RUNX2, OPN and OCN in C3H10T1/2 cells in PD group and SB group were significantly decreased (P< 0.05). The mRNA expression levels of RUNX2, OPN and OCN in C3H10T1/2 cells of PD+IGF-1 group and SB+IGF-1 group were significantly increased (P< 0.05). However, compared with IGF-1 group, the mRNA expression levels of RUNX2, OPN and OCN in C3H10T1/2 cells in PD+IGF-1 group and SB+IGF-1 group were significantly decreased (P< 0.05). Conclusion IGF-1 promotes osteogenic differentiation of C3H10T1/2 cells, and its mechanism may be related to the activation of ERK signaling pathway and p38 MAPK signaling pathway |