电针对大鼠脊髓损伤后细胞凋亡PARP-1全长影响的研究

The Effect of Electro-acupancture on PARP-1 of Cell Apoptosis after Spinal Cord Injury of Rats

目的:采用大鼠急性脊髓损伤模型,观察电针对脊髓损伤后神经细胞凋亡与其相关基因PARP-1全长表达影响及变化规律,试图从线粒体启动凋亡途径角度揭示电针治疗脊髓损伤作用机制。方法:急性脊髓损伤模型以Allen's法制备,将大鼠分为电针组、药物组(Caspase-3抑制剂组)、模型组、假手术组。对凋亡细胞采用Tunel法予以标记。结果:Tunel标记结果表明:脊髓损伤后6 h,PARP-1全长在模型组开始有表达,1 d表达量最高,在3 d、7 d逐渐下降,14 d最低。模型组在1 d、3 d表达量分别高于假手术组和药物组(P<0.05)。电针组在3 d表达量低于模型组(P<0.05)。结论:①细胞凋亡现象发生在大鼠急性脊髓损伤后,这是脊髓继发性损伤主要病理机制;②PARP-1全长在大鼠脊髓损伤后神经元中表达量随着时间推移逐渐增加,提示PARP-1全长可能参与了脊髓继发性损伤;③电针通过抑制PARP-1大鼠脊髓损伤神经元中PARP-1全长的表达,从而抑制了神经细胞的凋亡,减轻脊髓继发性损伤。

Objective：With the model rats of acute SCI,the paper investigates that the electro-acupuncture affects the expression of neural cell apoptosis and changes related genes for PARP-1 after spinal cord injury of rats.The paper tries to show that the mechanisms of electro-acupuncture on spinal cord injure and the study of related important factors of mitochondrion excitement apoptosis way.Methods：Acute spinal cord injury models by Allen＇s preparation,the rats were divided into acupuncture group and drug group（Caspase-3 inhibitor group）,model group,sham operation group.Apoptotic cells were marked by Tunel method.Results：Tunel labeling results showed that spinal cord injury after 6h,PARP-1 expression in the model group appeared,1d expression was the highest,on the 3 d,7 d it gradually decreased,on the 14 d it was the lowest.Model group expression levels were higher than that in sham operation group and drug group on the 1 d,3 d（P0.05）.Expression of electro-acupuncture group was lower than that in model group on the 3 d（P0.05）.Conclusion：First： Apoptosis occurs in rats after acute spinal cord injury.Spinal cord injury is the main pathological mechanism.Second： The expression of PARP-1 in rat neurons increased gradually after spinal cord injury,suggesting that PARP-1 may be involved in spinal cord injury.Third： Electro-acupuncture inhibits apoptosis of neural cells and reduces spinal cord injury by inhibiting neurons expression of PARP-1 in spinal cord injury.