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Upregulation of Cdh1 signaling in the hippocampus attenuates brain damage after transient global cerebral ischemia in rats
Neurochemistry international ( IF 4.2 ) Pub Date : 2017-07-12 , DOI: 10.1016/j.neuint.2017.07.005
Bo Zhang , Kai Wei , Xuan Li , Rong Hu , Jin Qiu , Yue Zhang , Wenlong Yao , Chuanhan Zhang , Chang Zhu

Cerebral ischemia is a major cause of brain dysfunction. The E3 ubiquitin ligase anaphase-promoting complex and its coactivator Cdh1 have been reported to be involved in the regulation of neuronal survival, differentiation, axonal growth and synaptic development in the central nervous system. However, its role in the ischemic brain and the underlying mechanisms remain poorly understood. The present study aimed to investigate the effects of Cdh1 overexpression on the ischemic rat brain by direct intra-hippocampal injection of lentivirus-delivered Cdh1 before transient global cerebral ischemia reperfusion. Spatial memory acquisition and retention were assessed using a Morris water maze task. Neuronal damage, glial activation, oxidative stress and the synaptic ultrastructure were also examined. The results indicated that a recombinant Cdh1-encoding lentiviral vector can upregulate the expression of Cdh1 in the rat hippocampus. Cdh1 overexpression increased the survival rates of rats, reversed the abnormal accumulation of cyclin B1, alleviated neuronal death, inhibited glial activation, mitigated oxidative stress, modulated synaptic plasticity and improved neurological deficits caused by ischemia. Our study indicates that targeting the Cdh1 signaling pathway in the hippocampus may provide a promising therapeutic strategy for the clinical treatment of transient global cerebral ischemia.



中文翻译:

大鼠短暂性全脑缺血后海马Cdh1信号的上调减轻了脑损伤

脑缺血是脑功能障碍的主要原因。据报道,E3泛素连接酶后期促进复合物及其辅助激活物Cdh1参与中枢神经系统神经元存活,分化,轴突生长和突触发育的调节。然而,其在缺血性脑中的作用及其潜在机制仍知之甚少。本研究旨在探讨在短暂性全脑缺血再灌注前,海马内直接注射慢病毒递送的Cdh1引起的Cdh1过表达对缺血大鼠脑的影响。使用莫里斯水迷宫任务评估空间记忆的获取和保留。还检查了神经元损伤,神经胶质活化,氧化应激和突触超微结构。结果表明,重组Cdh1编码慢病毒载体可以上调大鼠海马中Cdh1的表达。Cdh1过表达提高了大鼠的存活率,逆转了细胞周期蛋白B1的异常蓄积,减轻了神经元死亡,抑制了神经胶质活化,减轻了氧化应激,调节了突触可塑性,改善了缺血引起的神经功能缺损。我们的研究表明,针对海马中的Cdh1信号通路可能为临床治疗短暂性全脑缺血提供有希望的治疗策略。减轻氧化应激,调节突触可塑性并改善缺血引起的神经功能缺损。我们的研究表明,针对海马中的Cdh1信号通路可能为临床治疗短暂性全脑缺血提供有希望的治疗策略。减轻氧化应激,调节突触可塑性并改善缺血引起的神经功能缺损。我们的研究表明,针对海马中的Cdh1信号通路可能为临床治疗短暂性全脑缺血提供有希望的治疗策略。

更新日期:2017-07-12
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