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首页> 外文会议>2014 IEEE Workshop on Electronics, Computer and Applications >Ischemic preconditioning mediate NMDA receptors through downregulation of c-Jun activation and up-regulation of c-fos in hippocampus CA1
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Ischemic preconditioning mediate NMDA receptors through downregulation of c-Jun activation and up-regulation of c-fos in hippocampus CA1

机译：缺血预处理通过下调海马CA1的c-Jun激活和上调c-fos介导NMDA受体

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OBJECTIVE To explore the role of ERK5 and JNK3 in preconditioning regulation and protein expression with or without CIP and NMDA receptors mediate preconditioning-induced downregulation of c-Jun activation and up-regulation of c-fos in hippocampus CA1. METHODS: MK-801 (10 µM) was administered to rats by unilateral intracerebroventricular infusion (i.c.v.) 20 min prior to preconditioning. The rats were subjected to global cerebral ischemia (GCI) by four-vessel occlusion Rats were subjected to Sham operation (Sham), 8-min global cerebral ischemia + 3d reperfusion (R3d); ischemic preconditioning (P + R3d), ischemic preconditioning + saline + 3d reperfusion (saline), ischemic preconditioning + MK-801 pretreatment + 3d reperfusion (MK-801). Western blotting analysis of the effects of ERK5 and JNK3 in preconditioning regulation and protein expression with or without CIP in hippocampal CA1 regions. RESULTS: global cerebral ischemia significantly increased p-c-Jun as compared to Sham controls. In contrast, preconditioning abolished the global ischemia-induced elevation of p-c-Jun. The effect of preconditioning on p-c-Jun was significantly reversed by pretreatment with the ERK5-AS, while vehicle alone pretreatment had no effect. The changing trend of the C-fos expression was all opposite to that of p-cJun.; Semi-quantitative analysis of the levels of p-c-jun and c-fos levels from the different groups. The influence of ERK5-AS on protein binding activity of p-Bad in cytoplasm and 14-3-3 protein. Immunoprecipitation results showed that Preconditioning significantly increased the protein binding activity of p-Bad and 14-3-3 as compared to 8-min global cerebral ischemia. ERK5-AS apparent reversed the up-regulation. CONCLUSION global cerebral ischemia significantly increased p-c-Jun preconditioning abolished the global ischemia-induced elevation of p-c-Jun. Preconditioning significantly increased the protein binding activity of p-Bad and 14-3-3, ERK5-AS apparent reversed- the up-regulation.
机译：目的探讨ERK5和JNK3在有或没有CIP和NMDA受体的预处理调节和蛋白表达中的作用，介导预处理诱导的海马CA1 c-Jun激活下调和c-fos上调。方法：在预处理前20分钟，通过单侧脑室灌注（i.c.v.）向大鼠施用MK-801（10 µM）。通过四支血管闭塞对大鼠进行全脑缺血（GCI）。对大鼠进行Sham手术（Sham），8分钟的全脑缺血+ 3d再灌注（R3d）；缺血预处理（P + R3d），缺血预处理+盐水+ 3d再灌注（盐水），缺血预处理+ MK-801预处理+ 3d再灌注（MK-801）。蛋白质印迹分析ERK5和JNK3在海马CA1区是否有CIP的预处理调节和蛋白表达中的作用。结果：与假手术对照组相比，全脑缺血明显增加了p-c-Jun。相反，预处理消除了局部缺血引起的p-c-Jun升高。用ERK5-AS预处理可以显着逆转对p-c-Jun的预处理效果，而单独的媒介物预处理则无效果。 C-fos表达的变化趋势与p-cJun的变化趋势完全相反。半定量分析不同组中p-c-jun和c-fos的水平。 ERK5-AS对细胞质中p-Bad和14-3-3蛋白结合活性的影响。免疫沉淀结果显示，与8分钟的整体性脑缺血相比，预处理显着提高了p-Bad和14-3-3的蛋白结合活性。 ERK5-AS明显逆转了上调。结论全脑缺血明显增加了p-c-Jun预处理，从而消除了全脑缺血引起的p-c-Jun升高。预处理显着提高了p-Bad和14-3-3的蛋白结合活性，ERK5-AS明显逆转了上调。

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