脑损伤后JNK3基因参与神经细胞凋亡及神经功能恢复

发布时间：2018-02-05 19:24

本文关键词： JNK3 脑损伤细胞凋亡神经功能恢复　出处：《昆明医科大学》2013年硕士论文　论文类型：学位论文

【摘要】：目的：越来越多的证据表明脑损伤(traumatic brain injury, TBI)后c-Jun氨基末端激酶(c-Jun amino-terminal kinase, JNK)通路的激活参与神经细胞凋亡及神经功能恢复。然而,其是通过激活JNK家族中哪些基因发挥作用的呢?目前并不十分明确。因此,我们采取原位末端标记法(TdT-mediated dUTP Nick-End Labeling, TUNEL)、逆转录聚合酶链式反应(Reverse Transcription-Polymerase Chain Reaction, RT-PCR)、神经功能缺损评分(Neurological Severity Scores, NSS)等方法,探讨脑损伤大鼠JNK1, JNK2, JNK3基因表达变化、神经元凋亡及神经功能改变的关系。方法：取SPF级Sprague-dawly(SD)成年健康6月龄雄性大鼠100只,体质量220-260g,随机分为假手术组30只和脑损伤组70只(自由落体撞击法建立脑损伤模型)。RT-PCR检测：假手术组10只,脑损伤组分为1h组、6h组、1d组和7d组各取10只；损伤周边区皮质取材取材进行TUNEL染色：假手术组10只,脑损伤组分为6h组和7d组各取10只；用NSS评分评估神经功能的改变：假手术组和脑损伤组各取10只。结果：发现大鼠脑组织JNK3基因表达在TBI后1h、6h、1d和7d下降(P0.05),JNK1和JNK2的表达无明显变化(P0.05)。TUNEL染色显示：TBI后6h脑损伤周边区凋亡细胞数显著增多(P0.05),TBI后7d较伤后6h减少(P0.05),脑损伤皮质周边区凋亡神经细胞逐渐减少。大鼠神经功能缺损评分在脑损伤后1,3,5,7,14,28d逐渐降低,各时间点组间比较,差异有统计学意义(P0.05)；TBI组与假手术组比较,NSS评分明显增加(P0.05)。结论：JNK3在脑损伤后表达下调,可能与神经细胞凋亡相关,JNK3的下调可能促进脑损伤后神经功能的恢复。
[Abstract]:Objective : To investigate the effects of activation of c - Jun amino - terminal kinase ( p - c - Jun amino - terminal kinase ) via activation of c - Jun amino - terminal kinase in brain injury and the restoration of nerve function . However , it is not very clear about which genes are activated in the family of brain injury . Therefore , we have studied the relationship between the expression changes , neuronal apoptosis and nerve function changes in rats with brain injury by means of the method of in - situ end labeling ( tdT - mediated nick - End Labeling , TUNEL ) , Reverse Transcription - Polymerase Chain Reaction ( RT - PCR ) and neurological deficit scoring ( NSS ) . Methods : 100 male rats with SPF grade Sprague - Dawley ( SD ) were randomly divided into sham operation group ( 30 rats ) and brain injury group ( 70 rats ) . Results : There was no significant change in the expression of NK3 gene in brain tissue of rats ( P0.05 ) . The number of apoptotic cells in the peripheral area of brain injury was decreased significantly ( P0.05 ) . Conclusion : The down - regulation after brain injury may be related to neuronal apoptosis , and the down regulation may promote the recovery of neurological function after brain injury .

【学位授予单位】：昆明医科大学
【学位级别】：硕士
【学位授予年份】：2013
【分类号】：R651.15

【参考文献】