丙戊酸钠促进神经根回植术后神经元存活的机制研究

Neuroprotection Role of Sodium Valproate after Nerve Root Re-implantation

目的探讨丙戊酸钠对大鼠臂丛神经根回植术后脊髓神经元保护的作用机制。方法将成年大鼠随机分为空白组、手术组和丙戊酸钠组。手术组和丙戊酸钠组对大鼠行臂丛根性撕脱伤后神经根回植术,其中丙戊酸钠组通过饮水喂食丙戊酸钠。术后第1、2、3、7、14天收集相应节段脊髓,应用TUNEL法检测神经元凋亡情况,应用Western blot法及实时荧光定量PCR检测Bcl-2的表达情况。结果TUNEL法检测在术后第1、2天未发现凋亡细胞,术后第3~14天发现凋亡神经元,术后第3、7天丙戊酸钠组凋亡神经元个数少于手术组(P<0.05);应用Western blot法检测发现,术后第2、3、7天丙戊酸钠组Bcl-2的蛋白表达明显高于手术组(P<0.05);应用实时荧光定量PCR检测Bcl-2的mRNA表达发现,术后第2、3、7天丙戊酸钠组Bcl-2的mRNA表达明显高于手术组(P<0.05)。结论臂丛根性撕脱伤行神经根回植术后早期应用丙戊酸钠可以抑制神经元的凋亡,其机制可能是通过促进脊髓内部Bcl-2表达、抑制凋亡信号传导路径而实现的。

[WTHZ]Objective[WT][KG1]To explore the protective effect of Sodium valproate on spinal cord neurons in rats with brachial plexus root avulsion after nerve root re-implantation.Method Adult rats were randomly divided into three groups:blank group,operation group and valproate group.The operation group and the valproate group were treated with nerve root replantation after brachial plexus root avulsion injury,and the rats in valproate group was fed with Sodium volproate by drinking water after operation.The corresponding segments of spinal cord were collected at 1 d,2 d,3 d,7 d and 14 d after operation,then apoptotic of neurons was detected by TUNEL and the expression of Bcl-2 was detected by Western blot and real-time quantitative PCR.Results No apoptotic cells were found at 1 d and 2 d after surgery by TUNEL detection,and apoptotic neurons were found at 3 d to 14 d after surgery,the percentage of apoptotic neurons in the valproate group was less than that in the operation group at 3 d and 7 d after operation(P<0.05).It was found by Western blot that Bcl-2 protein expression in the valproate group was higher than that in the operation group at 2 d,3 d,7 d after operation(P<0.05).By Real-time PCR detection found Bcl-2 mRNA expression in valproate group is higher than that in operation group at 2 d,3 d,7 d after operation(P<0.05).Conclusion The early application of Sodium valproate can inhibit the apoptosis of neurons after the re-implantation of nerve roots in brachial plexus avulsion injury,and the mechanism may be achieved by promoting the expression of Bcl-2 in the spinal cord and inhibiting the apoptosis signal transduction pathway.