腺苷A1受体基因敲除小鼠致痫后海马神经细胞线粒体功能损伤的研究

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。

Mitochondrial Damage in Hippocampal Neurons in Adenosine A1 Receptor Knock-out Mice after Pentetrazole Kindling

Objective: To investigate mitochondrial damage in hippocampal neurons in adenosine A1 receptor knock-out mice after pentetrazole(PTZ) kindling.Methods: The adenosine 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 evident in hippocampal neurons at early stage of epilepsy.A1 adenosine receptor activation could attenuate this kind of mitochondrial damage in mice after epilepsy.