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

2014 IEEE Workshop on Electronics, Computer and Applications Pub Date : 2014-06-30 DOI:10.1109/IWECA.2014.6845784

Liu Jie, Zhang Ming, Zhu Ying

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引用次数: 0

摘要

目的探讨ERK5和JNK3在预处理调控中的作用，以及有或无CIP和NMDA受体介导的海马CA1中c-Jun激活下调和c-fos上调的蛋白表达。方法:大鼠预处理前20 min单侧脑室灌注MK-801 (10 μM)。大鼠进行假手术(Sham)， 8 min脑缺血+ 3d再灌注(R3d);缺血预处理(P + R3d)、缺血预处理+生理盐水+ 3d再灌注(saline)、缺血预处理+ MK-801预处理+ 3d再灌注(MK-801)。Western blotting分析ERK5和JNK3在有或无CIP海马CA1区预处理调控和蛋白表达中的作用。结果:与Sham对照组相比，全脑缺血显著增加p-c-Jun。相比之下，预处理可消除全脑缺血引起的p-c-Jun升高。ERK5-AS预处理显著逆转了预处理对p-c-Jun的影响，而单独预处理对p-c-Jun没有影响。C-fos表达量的变化趋势与p-cJun相反;半定量分析不同组p-c-jun和c-fos水平。ERK5-AS对细胞质中p-Bad蛋白和14-3-3蛋白结合活性的影响。免疫沉淀结果显示，与全脑缺血8 min相比，预处理显著提高了p-Bad和14-3-3蛋白结合活性。ERK5-AS明显逆转了上调。结论全脑缺血显著增加p-c-Jun预处理可消除全脑缺血引起的p-c-Jun升高。预处理显著提高了p-Bad和14-3-3蛋白结合活性，ERK5-AS明显逆转了上调。

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Ischemic preconditioning mediate NMDA receptors through downregulation of c-Jun activation and up-regulation of c-fos in hippocampus CA1

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.

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2014 IEEE Workshop on Electronics, Computer and Applications

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