Neuronal ERCC6 mRNA expression in rat brain induced by a transient focal cerebral ischemia

Neuronal ERCC6 mRNA expression in rat brain induced by a transient focal cerebral ischemia 1

目的：观察缺血再灌注损伤对转录修复耦联因子（ＥＲＣＣ６）ｍＲＮＡ表达水平的影响．方法：在大鼠大脑中动脉栓塞模型上结合Ｎｏｒｔｈｅｒｎ杂交，原位杂交和共聚焦激光扫描显微镜的方法观察脑内ＥＲＣＣ６ｍＲＮＡ的表达，并进行细胞定位分析．结果：缺血再灌注损伤后，在缺血中心及边周区的ＥＲＣＣ６ｍＲＮＡ表达，２天时开始增加，３天达峰值，７天开始下降．ＥＲＣＣ６ｍＲＮＡ主要在缺血侧的神经元上表达，少数在星型胶质细胞上表达．结论：缺血侧神经元和神经胶质细胞上ＥＲＣＣ６ｍＲＮＡ表达增加，这提示了损伤后神经细胞的ＤＮＡ自身修复能力被增强．

AIM: To study whether the excision repair cross complementing group 6 (ERCC6) is involved in the neuronal pathophysiological process following cerebral ischemia reperfusion injury. METH￣ODS: A transient middle cerebral artery occlusion (MCAO) was used to induce cerebral ischemia reperfusion injury in rat brain. Northern blot was used to check a specific signal for oligonucleotide probe. The expression of ERCC6 mRNA in the rat brain was observed by in situ hybridization. The specific cellular distribution of ERCC6 mRNA in the neuron or glia of the rat brain was analyzed by double staining combined with confocal laser scanning microscopic analysis. RESULT: The expres￣sion of ERCC6 mRNA in the penumbra area increased following ischemia and reperfusion with a time dependent manner. ERCC6 was express￣ed on d 2, reached peak values on d 3, and kept high level even on d 14 of reperfusion following ischemia. Number of ERCC6 mRNA expressive cell in the penumbra area on d 1, d 2, d 3, d 7, d 14 of reperfusion following ischemia were (0±0), (253±56), (816±355), (341±185), (128±95) ×10 6 cells/m 2, respec￣tively. Con￣fo￣cal micro￣scopic analysis showed that ERCC6 mRNA coexpress￣ed with phosphopyruvate hydra￣tase in the neurons and with glial fibrillary acidic protein (GFAP) in a few proliferation astrocyte glia. CONCLU￣SION: The expres￣sion of trans￣crip￣tion repair coupling factor ERCC6 mRNA in the neuron and glia was induced by ischemia reperfusion injury.