目的    探究Semaphorin3B(SEMA3B)在施万细胞调控周围神经损伤后华勒退变进程中的作用及分子机制。  方法    使用施万细胞敲除SEMA3B小鼠（cKO）为实验组，同窝Cre工具小鼠为对照组。通过体内横断坐骨神经和坐骨神经外植块培养分别建立体内和体外华勒退变模型，5d后取材开展免疫荧光染色和蛋白质印迹检测MBP、NF、c-Jun、MAG、p-AKT、AKT、p-GSK3β、GSK3β、p-ERK、ERK、p-JNK、JNK的表达差异，并用AKT激动剂在体外模型开展逆转验证实验。  结果    神经损伤5d后，cKO组体内外模型中MBP和NF的表达均高于Cre组，提示其华勒变性减慢。同时，cKO组的c-Jun表达下调而MAG表达量增高，提示施万细胞去分化程度降低；p-AKT和p-GSK3β表达下调，而p-ERK和p-JNK无显著差异；使用AKT激动剂(SC79)能逆转SEMA3B导致的MBP和NF的表达变化。  结论    施万细胞敲除SEMA3B后可以通过AKT/GSK3β信号通路延缓华勒变性过程。

Objective    To explore the role and mechanism of Semaphorin3B (SEMA3B) in Schwann cells during Wallerian degeneration in the injured peripheral nerve.    Methods    The Schwann cell specific SEMA3B knockout (cKO) mice and the littermate Cre mice were selected as an experimental group and a control group, respectively. The in vivo and in vitro models of Wallerian degeneration by nerve transection injury and nerve explant culture were prepared. Five days later, the tissues were collected to perform immunofluorescence and Western blotting with antibodies of MBP, NF, c-Jun, MAG, p-AKT, AKT, p- GSK3β, GSK3β, p-ERK, ERK, p-JNK, and JNK. Moreover, SC79 (the agonist of AKT) was used to perform the rescue experiment in the in vitro model.    Results    After 5 days of nerve injury, the expression of MBP and NF in both in vivo and in vitro models of the cKO group was higher than that of the Cre group, indicating Wallerian degeneration was delayed in the cKO group. Compared with the Cre group, the expression of c-Jun was lower and MAG was higher in the cKO group, suggesting that the Schwann cell dedifferentiation was reduced. The expression of p-AKT and p- GSK3β was down-regulated, while there was no significant difference in the levels of p-ERK and p-JNK. The administration of AKT agonist (SC79) could reverse the changes of MBP, and NF caused by SEMA3B cKO.    Conclusions    SEMA3B conditional knockdown in Schwann cells delay the Wallerian degeneration through inhibiting the AKT/ GSK3β pathway.