| ObjectivesFacial nerve injury has a very high incidence in cranial nerve diseases.Schwann cells,as myelin-forming cells of peripheral nerves,have been the focus of research on nerve injury and repair.CXCL12 is a chemokine factor that has been playing an important role since the embryonic period.While the role and mechanism of CXCL12 on facial nerve are still unclear.The main purpose of this study was to clarify the effects of CXCL12 on Schwann cells and facial nerves at cellular and animal levels,and further elaborate its mechanism.MethodsThe facial nerve injury models of rats were established artificially to observe the expression changes of CXCL12 after facial nerve injury.Then,the primary Schwann cells were extracted from the sciatic nerves of neonatal rats.After purification and identification,the effects of CXCL12 on Schwann cell proliferation,migration,cell cycle,apoptosis and autophagy were detected by different experimental methods.Besides,the changes of autophagy and major proteins in PI3K-AKT-m TOR pathway were detected by electron microscopy and Western blot.Finally,the injured facial nerves were treated with CXCL12,and the facial nerve function of the rats were evaluated by the change of facial nerve scores and the staining of HE,LFB and MBP.ResultsCXCL12 expression increased rapidly after facial nerve injury,peaked at 2 weeks,and returned to normal after 4 weeks.Cell experiments confirmed that CXCL12 had no significant effects on proliferation,cell cycle and apoptosis,but it could significantly promote the ability of migration.At the same time,CXCL12 could increase autophagy of Schwann cells through PI3K-AKT-m TOR pathway.Further animal experiments have found that CXCL12 can significantly reduce the functional scores of facial nerves and improve the degree of myelin loss.ConclusionCXCL12 can affect the migration of Schwann cells through the PI3K-AKT-m TOR pathway and promote the recovery of facial nerve function. |
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