Objective To study the effects of insulin-like growth factor-1 (IGF-1) on the proliferation,apoptosis and mitogen-activated protein kinase (MAPK) signaling pathway of rat colonic smooth muscle cells (SMCs).Methods Colonic SMCs in Sprague Dawley were isolated and cultured by enzymatic method.After immunohistochemical staining for identification of SMCs,SMCs were divided into control group,IGF-1 group,and IGF-1 + PD98059[extracellular signal-regulated kinase(ERK) inhibitor] group.3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) method was used for the detection of SMCs proliferation,flow cytometric Annexin V-FITC/PI for the detection of SMCs apoptosis,and Western blots for the detection of phosphorylated ERK,ERK,phosphorylated p38MAPK,p38MAPK and phosphorylated c-Jun N-terminal kinase(JNK),JNK expressions.Results The cultured cells were identified as colonic SMCs by immunohistochemical method.Compared with control group,cells proliferation of IGF-1 group was enhanced [(1.786 ± 0.271) vs.(0.998 ± 0.057),P ＜ 0.01],and apoptosis rate was reduced [(2.59 ± 0.28) ％ vs.(20.68 ±2.48) ％,P ＜ 0.01].Phosphorylated ERK expression in IGF-1 group was enhanced,and the ratio of phosphorylated ERK/ERK was increased [(42.71 ± 3.74) ％ vs.(23.88 ± 2.52) ％,all P ＜ 0.01].There were no differences for the expressions of phosphorylated p38MAPK,p38MAPK,phosphorylated JNK and JNK between IGF-1 group and control group (all P ＞ 0.05).Compared with control group,cells proliferation in IGF-1 ± PD98059 group was decreased significantly [(0.154 ± 0.021) vs.(0.998 ± 0.057),P ＜ 0.01],while apoptosis rate was increased [(84.31 ± 7.54) ％ vs.(20.68 ± 2.48) ％,P ＜ 0.01],phosphorylated ERK expression was reduced,and the ratio of phosphorylated ERK/ERK was decreased [(10.47 ± 1.22) ％ vs.(23.88 ± 2.52) ％,all P ＜ 0.01].Conclusion IGF-1 can promote the proliferation and inhibit apoptosis of colonic SMCs through activation of the ERK route of MAPK pathway,and p38MAPK and JNK routes may not be involved in this process.