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在匹罗卡品模型大鼠海马中的腺苷酸激酶 2 的动态表达。

Dynamic expression of adenylate kinase 2 in the hippocampus of pilocarpine model rats.

机构信息

Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.

出版信息

J Mol Neurosci. 2012 May;47(1):150-7. doi: 10.1007/s12031-011-9703-3. Epub 2012 Jan 14.

DOI:10.1007/s12031-011-9703-3
PMID:22246993
Abstract

Studies have shown that adenylate kinase 2 (AK2) is released from the mitochondrial inner membrane space during neuronal apoptosis, which plays an important role in temporal lobe epilepsy (TLE). We investigated the expression of AK2 in the hippocampus of a pilocarpine model rats. Using reverse transcription polymerase chain reaction and immunohistochemistry, AK2 mRNA and immune-positive cells were investigated during the entire epileptic process in pilocarpine-induced rat model of TLE. AK2 mRNA level was increased in rat hippocampus during different phases of the epileptogenesis, and reached a peak at 72 h. At 72 h time point, AK2 mRNA level was more than threefold comparing with the control. AK2-positive cells were observed in all regions of the hippocampus in model rats, but not in brain tissues of controls. The mean percentage of AK2-positive cells was increased as early as 6 h following seizure and reached a peak at 72 h. The pattern of AK2 expression over time was similar to that observed during neuronal apoptosis as detected with TUNEL staining. These results suggest that AK2 participates in the pathophysiological process of TLE and may be a marker for neuronal apoptosis induced by pathological injury in TLE.

摘要

研究表明,在神经元凋亡过程中,腺苷酸激酶 2(AK2)从线粒体内膜间隙释放出来,在颞叶癫痫(TLE)中发挥重要作用。我们研究了 AK2 在匹罗卡品诱导的 TLE 大鼠模型海马中的表达。采用逆转录聚合酶链反应和免疫组织化学方法,研究了 AK2 mRNA 和免疫阳性细胞在匹罗卡品诱导的 TLE 大鼠模型整个癫痫过程中的表达情况。AK2 mRNA 水平在癫痫发生的不同阶段均增加,并在 72 h 时达到峰值。在 72 h 时,AK2 mRNA 水平与对照组相比增加了三倍以上。在模型大鼠的海马体所有区域均观察到 AK2 阳性细胞,但在对照组的脑组织中未观察到。早在癫痫发作后 6 小时,AK2 阳性细胞的平均百分比就增加,并在 72 h 时达到峰值。AK2 表达的时间模式与 TUNEL 染色检测到的神经元凋亡过程相似。这些结果表明,AK2 参与了 TLE 的病理生理过程,可能是 TLE 中由病理性损伤诱导的神经元凋亡的标志物。

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本文引用的文献

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Mitochondrial dysfunction and oxidative stress in seizure-induced neuronal cell death.癫痫发作诱导的神经元细胞死亡中的线粒体功能障碍与氧化应激
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