虾青素通过sp1nr1通路拮抗mpp+诱导的pc12细胞氧化损伤

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1、分类号：R741.02学校代码：10392学科专业代码：100204学号：200901228福建医科大学硕士研究生毕业论文+虾青素通过Sp1/NR1通路拮抗MPP诱导的PC12细胞氧化损伤+AstaxanthinsuppressesMPP-inducedoxidativedamageinPC12cellsthroughaSp1/NR1signalingpathway学位类型：医学硕士所在学院：协和临床医学院研究生：张晓东学科、专业：神经病学导师：叶钦勇副教授研究起止日期：2010年11月至2012年3月答辩日期：2012年05月31日二○一二年六月万方数据万方数据目录英文缩略词表··

2、················································1中文摘要······················································2英文摘要······················································5前言························································7材料与方法····················································9结果·········

3、··············································21讨论·······················································28结论·······················································31参考文献·····················································32致谢·······················································36综述·········

4、··············································37万方数据英文缩略词表(Abbreviationsandacronyms)缩写英文全称中文全称ATXastaxanthin虾青素MPP+1-methyl-4-phenyl-pyridineion甲基苯基四氢吡啶离子NMDAN-Methyl-D-aspartatereceptorN-甲基天冬氨酸受体NR1NMDAreceptorsubunit1NMDA受体亚基1Sp1activatedtranscriptionfactor1激活转录因子1PDParkinsonDisease帕金森病ROSrea

5、ctiveoxygenspecies活性氧MITmithramycin光神霉素，Sp1抑制剂PMSFPhenylmethanesulfonylfluoride苯甲基磺酰氟Tris2-amino-2-hydroxymethyl-1,3-propanediol三羟甲基氨基甲烷PCRPolymerasechainreaction聚合酶链式反应ECLEnhancedchemiluminescence增强化学发光法1万方数据+虾青素通过Sp1/NR1通路拮抗MPP诱导的PC12细胞氧化损伤中文摘要【背景】帕金森病（ParkinsonDisease，PD）是老年人群中发病率很高的一种神经系统退行

6、性疾病，氧化应激损伤在帕金森病的发生中起着关键作用已被广泛认可。Sp1是第一个被克隆和纯化的核转录因子，具有高度保守的DNA结合序列。Sp1通过自身及其下游基因表达的调节参与多种细胞的增殖、凋亡及相关疾病的发生发展和治疗。体内外实验研究均证实，氧化应激条件下，Sp1的表达及其与NR1启动子结合活性均上调，进而上调NR1的表达，介导后续的兴奋毒性及细胞凋亡。N-甲基-D-天门冬氨酸(NMDA)受体在神经系统疾病中的作用越来越受到关注。NMDA受体主要存在突触前膜，是由NR1、NR2A-D、NR3A-B等亚单位构成的异四聚体。NR1是功能性NMDA受体的必须基团，PC12细胞中主要表达N

7、R1。氧化应激后，兴奋性谷氨酸过度激活NMDA受体导致神经元胞内钙超载而触发的系列生化改变和诱导相关基因的表达可能是导致神经元损伤的重要原因，因此该受体通道的调控在氧化应激的治疗中可能是重要的靶点之一。近年来发现虾青素（astaxanthin，ATX）具有显著的抗氧化损伤、清除自由基、抗凋亡等生物学作用，可顺利通过血脑屏障，有望成为治疗神经退行性疾病+的保护性药物。Sp1/NR1细胞信号通路在MPP诱导的PC12细胞氧化应激损伤+中作用未见报道，ATX是否