烟酰胺单核苷酸腺苷酰转移酶1（NMNAT1）对MES23.5帕金森病细胞模型的保护作用

发布时间：2018-06-30 06:23

本文选题：烟酰胺单核苷酸腺苷酰转移酶1 + 基因高表达　；参考：《青岛大学》2014年硕士论文

【摘要】：目的：探讨烟酰胺单核苷酸腺苷酰转移酶1(NMNAT1)基因表达对帕金森病(PD)细胞模型MES23.5细胞轴突长度及半胱氨酸蛋白酶3(Caspase3)、超氧化物歧化酶1(SOD1)表达的影响。方法：应用细胞转染、免疫荧光及Western印迹分析等方法,在制作PD细胞模型前向12孔板内分别转染NMNAT1高表达空载质粒、NMNAT1高表达质粒、NMNAT1干扰空载质粒及NMNAT1干扰质粒,并检测NMNAT1高表达正常组、高表达阳性组、高表达阴性组、NMNAT1干扰正常组、干扰阳性组和干扰阴性组以上6组MES23.5细胞轴突长度变化及Caspase3蛋白、SOD1蛋白的半定量表达。结果：与NMNAT1高表达(干扰)正常组比较,NMNAT1高表达(干扰)阴性组细胞轴突长度显著缩短,且其Caspase3表达量明显增加,SOD1表达量减少,差别具有统计学意义；与NMNAT1高表达(干扰)阴性组比较,NMNAT1高表达阳性组细胞轴突长度明显延长,且Caspase3表达量显著下降,SOD1表达量增加,差别具有统计学意义,NMNAT1干扰阳性组轴突长度变短,Caspase3表达量上升,SOD1表达量下降,差别具有统计学意义。结论：细胞凋亡及氧化应激在PD轴突损伤过程中发挥重要作用,而NMNAT1能够有效抑制凋亡蛋白Caspase3表达、增加SOD1表达,并明显延缓轴索损伤,从而在一定程度上具有神经保护作用。
[Abstract]:Objective : To investigate the effect of nicotinamide monnucleotide adenyltransferase 1 ( NMNAT1 ) gene expression on the axonal length and the expression of cysteine proteinase 3 ( caspase3 ) and superoxide dismutase ( SOD1 ) in Parkinson ' s disease ( PD ) cell model .

Methods : NMNAT1 high expression no - load plasmid , NMNAT1 high expression plasmid , NMNAT1 interfering empty plasmid and NMNAT1 interference plasmid were transfected into 12 well plates by cell transfection , immunofluorescence and Western blot analysis .

Results : Compared with the normal group of NMNAT1 high expression ( interference ) , the length of the axon of NMNAT1 high expression ( interference ) negative group was significantly shortened , and the expression of caspase3 increased significantly , the expression of SOD1 decreased , and the difference was statistically significant .
Compared with the NMNAT1 high expression ( interference ) negative group , the length of the axon of NMNAT1 high expression positive group was obviously prolonged , and the expression level of caspase3 was significantly decreased , the expression of SOD1 increased , the difference was statistically significant , the expression level of the NMNAT1 interference positive group was shortened , the expression level of Caspase3 increased , and the expression level of SOD1 decreased , and the difference was statistically significant .

Conclusion : Apoptosis and oxidative stress play an important role in PD axonal injury . NMNAT1 can effectively inhibit the expression of apoptosis protein Caspase3 , increase expression of SOD1 , and delay axonal injury .
【学位授予单位】：青岛大学
【学位级别】：硕士
【学位授予年份】：2014
【分类号】：R742.5

【共引文献】