大鼠脊髓半切损伤后SynDIG1对神经的修复作用

Neuroprotective effect of SynDIG1 on rat spinal cord hemisection injury

目的探讨Syn DIG1是否在突触重塑过程中对神经具有保护修复作用。方法建立大鼠脊髓半切损伤模型,将其分为治疗组和对照组,治疗组使用微渗透泵鞘内注射Syn DIG1蛋白,对照组注射等量的生理盐水。分别在24 h、7 d、42 d处死,进行HE染色、免疫组织化学染色(AMPAR、Caspase-3、TNF-α)和免疫荧光染色(MOP-FITC、CD45-PE、CD68-PE、GAP-43-PE)。结果 Syn DIG1治疗能够减少囊性空腔的形成,降低神经细胞凋亡相关因子Caspase-3、TNF-α和炎性相关因子MPO、CD45、CD68的表达,表明Syn DIG1能够减少神经元的死亡,减弱组织损伤,减轻机体炎症反应;同时,Syn DIG1能够提高神经修复相关蛋白AMPAR、GAP-43的含量,促进神经系统的修复、突触的形成。每周对大鼠的运动功能评分也显示,自术后2周起Syn DIG1治疗组的运动能力得到显著提高。结论 Syn DIG1蛋白在突触重塑、神经修复中起重要作用。

To study the neuroprotective effect of Syn DIG1, a rat spinal cord hemisection model wasestablished. The rats were divided into the treatment group and control group. The rats in the treatment group weregiven micro-osmotic pump intrathecal injection of Syn DIG1 protein, while the rats in the control group were injectedwith isometric normal saline. The animals were sacrificed at 24 h, 7 d and 42 d after treatment, and sections wereprepared for performing HE staining, immunohistochemical staining（AMPAR, Caspase-3 and TNF- alpha） andimmunofluorescence staining（MOP-FITC, CD45-PE, CD68-PE and GAP-43-PE）. Data showed that Syn DIG1 protein could significantly reduce neuronal death and alleviate inflammatory reaction, and reduce the expression ofCaspase-3, TNF-α, MPO, CD45, and CD68. Meanwhile Syn DIG1 also could improve the repair of nervous systemand the formation of synapse by means of improving the content of AMPAR and GAP-43. The weekly motor functionscore of rats also showed that the motor abilities of the rats in the treatment group were improved. The experimentalresults showed that Syn DIG1 protein has a neuroprotective and neuronal repair effect.