Zhao Zhiwei, Li Xiaoling, Li Qing
Luoyang Orthopedic Hospital of Henan Province, Zhengzhou 450046, Henan Province, China.
Luoyang Orthopedic Hospital of Henan Province, Zhengzhou 450046, Henan Province, China.
Biomed Pharmacother. 2017 Aug;92:1103-1110. doi: 10.1016/j.biopha.2017.05.099. Epub 2017 Jun 12.
Schwann cells (SCs) play an indispensable role in the repair and regeneration of injured peripheral nerve. Curcumin can reduce SCs apoptosis, and promote the regeneration and functional recovery of injured peripheral nerves. However, the corresponding mechanisms are not clear.
The article was aimed to explore the effect and corresponding mechanisms of curcumin on the repair of sciatic nerve injury in rats.
After surgery induced sciatic nerve injury, the model rats were divided into three groups and treated with curcumin, curcumin+PD98059 and curcumin+IGF-1 respectively for 4days. The phosphorylation of Erk1/2 and Akt, and the expression of LC3-II, Beclin 1 and p62 were measured using western blotting. After treatment for 60days, myelination of the injured sciatic nerve was evaluated by MBP immunohistochemical staining and the expression of PMP22, Fibrin and S100 were determined using qRT-PCR and western blotting. In vitro, RSC96 cells were starved for 12h to induce autophagy, and received DMSO, curcumin, PD98059+curcumin, IGF-1+curcumin and BFA1 respectively. The phosphorylation of Erk1/2、Akt and the expression of LC3-II, Beclin 1, p62, PMP22, Fibrin and S100 were measured using western blotting, and the cell apoptosis was detected by flow cytometry.
Curcumin could promote injury-induced cell autophagy, remyelination and axon regeneration in sciatic nerve of rats. In vitro, curcumin could accelerate cell autophagy through regulating autophagy related Erk1/2 and Akt pathway, prevent cell apoptosis and promote expression of PMP22 and S100, and reduced deposition of Fibrin in cultured RSC96 SCs.
Curcumin could accelerate injured sciatic nerve repair in rats through reducing SCs apoptosis and promoting myelinization.
施万细胞（SCs）在损伤的周围神经修复和再生中发挥着不可或缺的作用。姜黄素可减少施万细胞凋亡，促进损伤的周围神经再生和功能恢复。然而，其相应机制尚不清楚。
探讨姜黄素对大鼠坐骨神经损伤修复的作用及相应机制。
手术诱导大鼠坐骨神经损伤后，将模型大鼠分为三组，分别给予姜黄素、姜黄素+PD98059和姜黄素+IGF-1处理4天。采用蛋白质印迹法检测Erk1/2和Akt的磷酸化水平，以及LC3-II、Beclin 1和p62的表达。处理60天后，通过髓鞘碱性蛋白（MBP）免疫组织化学染色评估损伤坐骨神经的髓鞘形成情况，并采用实时荧光定量聚合酶链反应（qRT-PCR）和蛋白质印迹法检测外周髓鞘蛋白22（PMP22）、纤维蛋白原（Fibrin）和S100的表达。体外实验中，将大鼠施万细胞系（RSC96）细胞饥饿12小时以诱导自噬，分别给予二甲基亚砜（DMSO）、姜黄素、PD98059+姜黄素、IGF-1+姜黄素和巴弗洛霉素A1（BFA1）处理。采用蛋白质印迹法检测Erk1/2、Akt的磷酸化水平，以及LC3-II、Beclin 1、p62、PMP22、Fibrin和S100的表达，采用流式细胞术检测细胞凋亡情况。
姜黄素可促进大鼠坐骨神经损伤诱导的细胞自噬、髓鞘再生和轴突再生。体外实验中，姜黄素可通过调节自噬相关的Erk1/2和Akt信号通路加速细胞自噬，防止细胞凋亡，促进PMP22和S100的表达，并减少培养的RSC96施万细胞中纤维蛋白原的沉积。
姜黄素可通过减少施万细胞凋亡和促进髓鞘形成加速大鼠损伤坐骨神经的修复。
