神经电刺激对大鼠脊髓钝挫伤后神经营养因子4和增殖细胞核抗原表达影响的研究

关键词：脊髓损伤  神经电刺激  神经生长因子家族  增殖细胞核抗原

Keywords:spinal cord injury  nerve electrical stimulation  nerve growth factor families  proliferating cell nuclear antigen

摘要：

      摘要 目的：探讨在电刺激干预下大鼠脊髓损伤节段神经生长因子（NT4）和增殖细胞核抗原（PCNA）的表达及对脊髓损伤的影响。 方法：成年雌性SD大鼠78只，随机分为3组：假手术组（n=6）、对照组（n=36）和实验组（n=36）。Allen's法复制SD大鼠T9脊髓钝挫伤模型。实验组脊髓钝挫伤后给予夹脊穴和足三里穴位神经电刺激干预。神经行为学评分后，运用免疫组化和蛋白质印迹（Western blot）来检测NT4、PCNA的表达变化。 结果：行为学观察，实验组大鼠术后1周BBB评分显著高于对照组（P＜0.05），低于假手术组（P＜0.05）。实验组第1—3天NT4表达显著升高（P＜0.05），第7天达到峰值并且其表达明显高于对照组（P＜0.05）。实验组第1—3天PCNA表达降低，第7天达到最大差异（P＜0.05）。 结论：电刺激干预下，脊髓组织中神经元中的NT4表达增强，电刺激能改善运动功能恢复。神经电刺激后PCNA表达减少，神经电刺激对神经干细胞的分化作用大于神经干细胞的再生增殖。

Abstract:

      Abstract Objective: To explore the impacts of nerve electrical stimulation on the expressions of neurotrophin-4（NT4） and proliferating cell nuclear antigen（PCNA） after spinal cord contusion in SD rats. Method: Seventy-eight adult female SD rats were randomly divided into three groups: sham group (n=6), control group (n=36) and experimental group (n=36). SD rats were prepared according to Allen's method for T9 spinal cord contusion. Experimental group was given Jiaji（EX-B2） point and Zusanli（ST36） point nerve electrical stimulation intervention after spinal cord contusion (SCC). After neurobehavioral score assessment, immunohistochemistry and Western blot were used to detect the expressions of NT4 and PCNA at different time and in different groups. Result: After spinal cord contusion on the 1st—3rd d SD rats, BBB score increased gradually, compared with control group, on the 7th d BBB score of experimental group restored significantly(P＜0.05). Immunohistochemistry and Western blot analysis showed that the experimental group compared with control group, NT4 expression raised, and reached the maximum difference until the 7th d (P＜0.05). PCNA expression depressed, and reached the maximum difference until the 7th d(P＜0.05). Conclusion: Nerve electrical stimulation can promote the expression of NT4 but not PCNA that may create nerve regeneration microenvironment which contribute to the recovery of hindlimb motor function in rats.