摘要
目的:观察腺苷A1受体基因敲除小鼠戊四氮致痫后海马神经细胞线粒体功能的损伤。方法:腺苷A1受体基因敲除小鼠和野生型小鼠各30只,各随机分为对照组、致痫后6h、24h、7d、30d组,每组6只;戊四氮点燃制作癫痫模型;于各时间点取小鼠海马,流式细胞仪测线粒体膜电位,免疫荧光测细胞色素C(cyt C)的表达。结果:基因敲除小鼠和野生型小鼠致痫后6h、24h、7d及30d组的线粒体膜电位均低于对照组(P<0.05),cyt C释放量均高于对照组(P<0.05);除对照组外,基因敲除小鼠致痫后6h、24h、7d及30d组的线粒体膜电位均低于野生型小鼠(P<0.05),cyt C释放量均高于野生型小鼠(P<0.05)。结论:癫痫早期即可出现海马线粒体功能损伤,腺苷A1受体有助于减轻癫痫小鼠海马线粒体损伤。
Objective： To investigate mitochondrial damage in hippocarnpal neurons in adenosine A1 receptor knock-out mice after pentetrazole （PTZ） kindling. Methods： The adeno- sine A1 receptor knock-out （KO） mice （n=30） and wild type （WT） mice （n=30） were randomly divided into control group and 6 h, 24 h, 7 d and 30 d post-epilepsy groups （n=5,respectively）. Kindling model of epilepsy was induced by intraperitoneal injection of PTZ. Flow cytometry was used to detect mitochondria membrane potentials and immunofluorescence was applied to measure cytochrome C activity. Results： Compared with those in the control group, the mitochondria membrane potentials were significantly lower and the cytochrome C activity was higher in all the post-epilepsy groups （P^0.05）, both in KO mice and WT mice. Compared with those in the WT mice, the mitochondria membrane potentials were lower and the cytochrome C activity was higher in all the KO mice after epilepsy （P^0.05）. Conclusion： The mitochondrial damage is ev- ident in hippocampal neurons at early stage of epilepsy. A1 adenosine receptor activation could at- tenuate this kind of mitochondrial damage in mice after epilepsy.
出处
《神经损伤与功能重建》
2012年第6期400-402,435,共4页
Neural Injury and Functional Reconstruction
基金
国家自然科学基金(No.30770752)
关键词
腺苷A1受体
癫痫
海马
线粒体膜电位
细胞色素C
A1 adenosine receptor
epilepsy
hippocampus
mitochondria membrane po- tentials
cytochrome C
