帕金森模型大鼠脑内儿茶酚胺异喹啉类化合物的形成与代谢  

Formation and Metabolism of Catecholamine Isoquinolines in the 6-OHDA Lesion Rat Model Brains

作　　者：牟晓玲[1] 李丽莉[1] 朱勇[1] 张天[1] 魏玉霞[1] 马英[1] 邓玉林[1] 

机构地区：[1]北京理工大学生命科学与技术学院

出　　处：《化学通报》2008年第6期439-442,共4页Chemistry

基　　金：国家自然科学基金项目(20435020);民用航天课题项目(D2220062902)资助

摘　　要：帕金森(PD)是一种常见的神经退行性疾病,确切的致病机理尚不清楚,其中环境因素引起的神经毒素假说受到广泛关注。本文提出了关于内源性神经毒素恶性循环导致PD的假说。为了验证该假说,建立了定位注射6-OHDA单侧损毁黑质-纹状体的PD Wistar大鼠模型,并采用HPLC-ESI-TOF分别检测了PD模型大鼠和对照组大鼠脑健侧和受损侧的黑质、纹状体中Sal和NMSal的含量。结果表明,PD模型大鼠受损侧黑质-纹状体中Sal和NMSal的含量都比健侧及其他对照组高,说明PD模型受损侧内源性儿茶酚胺异喹啉类神经毒素导致的恶性循环严重,对假说的验证提供了依据。Parkinson＇ s disease （PD） is progressive neurodegenerative disorder and the exactly mechanism is still unknown. The extregenous and endogenous neurotoxin provoked by environmental factors may contribute to the development of PD and drew more and more attention. Based on our research data, a hypothesis of PD pathogenesis that CAIQs and related enzymes were involved in the dopaminergic neurons death had been proposed. In order to verify this hypothesis, the 6-OHDA lesion rat model was established and a method based on HPLC- ESI-TOF was developed for the determination of Sal and NMSal in nigra-striatum. Data showed that the Sal and NMSal in damaged regions of PD significantly raised （P 〈 0.05） compared to the control group, which firmly support the suggested hypothesis.

关 键 词：帕金森病 内源性神经毒素 儿茶酚胺异喹啉 

分 类 号：R742.5[医药卫生—神经病学与精神病学]