DL-3-n-butylphthalide promotes dendrite development in cortical neurons subjected to oxygen-glucose deprivation/reperfusion
DL-3-n-butylphthalide promotes dendrite development in cortical neurons subjected to oxygen-glucose deprivation/reperfusion
复制标题
DL-3-n-丁基苯酞促进缺氧/再灌注皮质神经元的树突发育
DOI：
10.1002/cbin.10980
复制
发表时间：
2018-08-01
影响因子：
3.9
通讯作者：
Wu, Cuiying
中科院分区：
文献类型：
--
作者：
Zhang, Peng;Xu, Ruxiang;Wu, Cuiying
功能恢复程度有限与缺血性脑卒中后梗死周围皮质的状况密切相关。培养神经元的氧糖剥夺模型可以部分模拟这种状况。适当的树突形态对于神经元功能的正确连接至关重要。因此，如何促进神经树突的可塑性这一问题具有重要意义。丁苯酞是一种治疗缺血性脑卒中的有效药物。在本研究中，丁苯酞除了具有神经保护作用外，经Sholl分析证实，它还可以增加一级和二级树突以及树突尖端的数量。本研究进一步表明，丁苯酞（DL - NBP）通过抑制PI3K/AKT信号通路正向调节树突分支。
The limited degree of functional recovery is closely associated with the condition of the periinfarct cortex after ischemic stroke. The model of oxygen-glucose deprivation in cultured neurons could partly simulate this condition. Proper dendritic morphology is crucial for the correct wiring of neuronal function. Hence, the question of how to facilitate the plasticity of neural dendrites is of great significance. DL-3-n-butylphthalide is an efficient medication for ischemic stroke. In this study, in addition to having neuroprotective effects, DL-3-n-butylphthalide could increase the number of primary and secondary dendrites and of dendritic tips as confirmed by Sholl analysis. This study further demonstrated that DL-NBP inactivates PI3K/AKT signaling to positively regulate dendritic branching.