Decreased nuclear factor-κB DNA binding activity following permanent focal cerebral ischaemia in the rat
Decreased nuclear factor-κB DNA binding activity following permanent focal cerebral ischaemia in the rat
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DOI：
10.1016/s0304-3940(00)01203-9
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发表时间：
2000-07-07
影响因子：
2.5
通讯作者：
Parsons, AA
中科院分区：
文献类型：
--
作者：
Irving, EA;Hadingham, SJ;Parsons, AA
许多与脑缺血发病机制有关的因子如谷氨酸、肿瘤坏死因子和白细胞介素-1已被证明能激活核因子-κ B（NF-κ B）。在本研究中，我们研究了NF-κ B B活性在不同的时间后，永久性局灶性脑缺血大鼠使用免疫组织化学，蛋白质印迹和电泳迁移率分析（EMSA）。采用免疫组化和蛋白质印迹法检测大脑中动脉闭塞后3 h NF-κ B B核转位。这反映在与组织学正常组织相比，缺血皮质中NF-κ B结合活性（EMSA）增加的趋势中。然而，与此相反，从6至48小时后闭塞核转位和NF-κ B B结合活性降低缺血皮质。在退化神经元中检测到NF-κ B结合活性降低，表明NF-κ B活性降低可能加剧缺血诱导的神经元细胞死亡。(C)2000 Elsevier Science爱尔兰有限公司保留所有权利。
Many factors implicated in the pathogenesis of cerebral ischaemia such as glutamate, tumour necrosis factor and interleukin-1 have a Iso been shown to activate nuclear factor-kappa B (NF-kappa B). In the present study we have investigated NF-kappa B activity at various times following permanent focal cerebral ischaemia in rats using immunohistochemistry, western blotting and electrophoretic mobility sh ift assay (EMSA). Three hours following middle cerebral artery occlusion nuclear translocation of NF-kappa B was detected using immunohistochemical and western blotting techniques. This was reflected in a trend towards increased NF-kappa B binding activity (EMSA) in the ischaemic cortex compared to histologically normal tissue. In contrast however, from 6 to 48 h post-occlusion nuclear translocation and NF-kappa B binding activity was decreased in the ischaemic cortex. Decreased NF-kappa B binding activity detected in degenerating neurones, suggests that decreased NF-kappa B activity may exacerbate ischaemia induced neuronal cell death. (C) 2000 Elsevier Science Ireland Ltd. Ail rights reserved.