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目的:通过体外培养神经细胞(SH-SY5Y)观察FK1706对神经细胞再生的作用并探讨其机制。方法:体外培养SH-SY5Y细胞，根据不同处理分别分为FK1706组、神经生长因子组(NGF)、FK1706＋NGF组、FK1706＋NGF＋格尔德霉素(Geldanamycin)组和空白对照组。细胞计数试剂盒(CCK-8)检测不同组细胞增殖活性，测量细胞轴突长度。分子生物学检测不同细胞中磷酸化促分裂原活化蛋白激酶激酶激酶(p-Raf)、磷酸化细胞外调节蛋白激酶(p-ERK)、p-Raf/Raf及p-ERK/ERK表达水平。通过免疫共沉淀(IP)检测不同细胞中热休克蛋白90(HSP90)与Raf结合的复合体表达水平。使用方差分析比较各组间数据。结果:CCK-8检测显示FK1706＋NGF组细胞增殖活性最强(1.12±0.08)，高于FK1706组和NGF组(0.61±0.07、0.89±0.04)，差异有统计学意义(n t＝6.824，n P<0.05)，加入格尔德霉素可以抑制其增殖活性(0.31±0.02)；FK1706＋NGF组细胞轴突最长，轴突长度为(277.40±18.64) μm，高于FK1706组和NGF组[(71.24±6.12)、(144.61±11.20) μm]，差异有统计学意义(n t＝14.577，n P<0.05)，FK1706＋NGF＋格尔德霉素组轴突长度[(97.06±11.29) μm]低于FK1706＋NGF组；NGF组p-Raf、p-ERK表达水平分别为(0.58±0.02)和(1.24±0.03)，高于对照组(0.25±0.03、0.76±0.02)和FK1706组(0.23±0.02、0.78±0.03，n t1＝23.335，n t2＝9.163，n P<0.05)，差异有统计学意义，加入FK1706可以增强NGF组p-Raf和p-ERK的表达水平(n t1＝21.213，n t2＝2.191，n P<0.05)，差异有统计学意义，加入格尔德霉素可以抑制FK1706和NGF的协同作用，与细胞轴突长度和增殖活性检测结果一致。IP检测显示FK1706＋NGF组HSP90/Raf复合体相对表达水平最高(1.56±0.04)，显著高于其他组(n t＝16.398，n P<0.05)，差异有统计学意义，FK1706＋NGF＋格尔德霉素组HSP90/Raf的表达水平(0.93±0.05)低于FK1706组和FK1706＋NGF组。n 结论:FK1706可以促进HSP90和Raf结合，提高大鼠肉瘤/促分裂原活化蛋白激酶激酶激酶/促分裂原活化蛋白激酶/细胞外调节蛋白激酶(Ras/Raf/MAPK/ERK)信号通路中Raf和ERK磷酸化水平，促进神经细胞增殖和轴突生长。“,”Objective:The effects and mechanism of FK1706 on nerve cell regeneration were observed through vitro cultured neural cells (SH-SY5Y).Methods:Vitro cultured SH-SY5Y cells were divided into FK1706 group, nerve growth factor (NGF) group, FK1706+ NGF group, FK1706+ NGF+ Geldanamycin group, and control group according to different treatments. The cells proliferation activity of different groups was detected by cell counting kit-8 (CCK-8) assay and the axonal length for SH-SY5Y cells of different groups was measured. The expression levels of phosphorylated-mitogen-activated protein kinases kinases kinases (p-Raf), phosphorylated-extracellular regulated protein kinases (p-ERK), p-Raf/Raf and p-ERK/ERK were detected in different cells through molecular biology. The expression level of the complex combined with heat shock protein 90 (HSP90) and Raf in different cells was detected through immunoprecipitation (IP). Analysis of variance was used to compare data between groups.Least-significant difference test was used for futher pairwise comparison.Results:CCK-8 assay showed that the cells proliferation activity was strongest in FK1706+ NGF group (1.12±0.08), significantly higher than in FK1706 (0.61±0.07) and NGF (0.89±0.04) groups (n t=6.824, n P<0.05). The proliferation sctivity of neural cells could be inhibited by Geldanamycin (0.31±0.02). The axonal length was longest in FK1706+ NGF group [(277.40±18.64) μm], compared to FK1706 group [(71.24±6.12) μm]and NGF group [(144.61±11.20)μm] (n t=14.577, n P<0.05). The axonal growth was inhibited by Geldanamycin (97.06±11.29)μm]. The expression levels of p-Raf (0.58±0.02) and p-ERK (1.24±0.03) in NGF group were higher than in control group [(0.25±0.03, 0.76±0.02) and FK1706 group (0.23±0.02, 0.78±0.03) (n t1=23.335, n t2=9.163, n P<0.05). Adding FK1706 could enhance the expression levels of p-Raf and p-ERK in NGF group (n t1=21.213, n t2=2.191, n P<0.05) and adding Geldanamycin could inhibit the synergy action between FK1706 and NGF, which were consistent with the results of cell axon length and proliferation activity. The HSP90/Raf complex expressions level was the highest (1.56±0.04) in FK1706+ NGF group (n t=16.398, n P<0.05). The HSP90/Raf complex expression level in FK1706+ NGF group could be reduced (0.93±0.05) by Geldanamycin.n Conclusion:FK1706 could promote the combination of FK1706 and Raf to increase the phosphate levels of Raf and ERK in the Ras/Raf/MAPK/ERK signaling path, and enhance nerve cell proliferation and axon growth.