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作 者:马琪林[1] 鲁丛霞[1] 蔡琰[2] 苏敏[2] 林其谁[3]
机构地区:[1]福建医科大学附属厦门第一医院神经内科,福建厦门361003 [2]上海交通大学仁济医院神经内科,上海200001 [3]中国科学院上海生化研究所分子生物学国家重点实验室,上海200031
出 处:《新乡医学院学报》2007年第2期114-116,共3页Journal of Xinxiang Medical University
基 金:卫生部科研基金资助项目(编号:96-2-294)
摘 要:目的探讨线粒体复合物活性和谷氨酸载体功能在帕金森病(PD)发病机制中的作用。方法首先提取帕金森病患者的血小板线粒体,测定复合物Ⅰ、Ⅱ、Ⅲ、Ⅳ的活性,然后先后用谷氨酸和草酰乙酸进一步装载线粒体,加入14C-谷氨酸后启动谷氨酸载体的转运,同时测定该载体的活性。结果与健康对照组相比,PD患者的血小板计数无明显变化(P>0.05),但线粒体复合物I的活性和谷氨酸载体的活性明显降低(P<0.05)。结论线粒体复合物和谷氨酸载体活性的改变参与了PD的发病机制。Objective To investigate the roles of glutamate carriers and complex of mitochondria in the pathogenesy of Parkinson's disease (PD). Methods The platelet mitochandria of patients with PD were extracted and the activities of complex Ⅰ, Ⅱ, Ⅲ and Ⅳ were detected, and then the mitochondria were loaded with glutamate and oxaloacetic acid respectively, finally to trigger the transporting of the glutamate carrier by adding the ^14C-glutamate and determine the activities of the carriers. Results There was no significantly change about the platelet counts of patients with PD compared with the healthy control( P 〉0.05 ), but the activities of glutamate carrier and complex of the mitochondria in the patients with PD were obviously reduced ( P 〈 0.05 ). Conclusion The claanges of activities of mitochondrial glutamate carrier and complex were involved in the pathogenesis of Parkinson's disease.
分 类 号:R742[医药卫生—神经病学与精神病学]
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