Melatonin exerts protective effect on N2a cells under hypoxia conditions through Zip1/ERK pathway
Melatonin exerts protective effect on N2a cells under hypoxia conditions through Zip1/ERK pathway
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DOI：
10.1016/j.neulet.2015.04.013
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发表时间：
2015-05-19
影响因子：
2.5
通讯作者：
Hou, Ming-xiao
中科院分区：
文献类型：
--
作者：
Liu, Xin-Wei;Zi, Ying;Hou, Ming-xiao
褪黑素在不同的中枢神经系统损伤中发挥神经保护作用。然而，褪黑激素神经保护作用的分子机制还不清楚。本实验研究了褪黑素对缺氧诱导的N2 a细胞的影响，结果表明褪黑素不仅能降低缺氧诱导的N2 a细胞中ROS和MDA的水平，诱导SOD的升高，还能促进细胞增殖，抑制细胞凋亡。此外，我们发现褪黑激素可以通过上调Zip 1的表达来激活MAPK/ERK通路。因此，本研究为褪黑素的作用机制提供了新的思路，有待于我们进一步的深入研究。(C)2015爱思唯尔爱尔兰有限公司版权所有。
Melatonin plays a neuroprotective role in different CNS injuries. However, the molecular mechanisms underlying neuroprotection by melatonin are not well understood. Here, we studied the effects of melatonin in hypoxia-induced N2a cells and our results demonstrated that melatonin not only reduced the level of ROS and MDA, induced the increase of SOD, but also increased the cell proliferation and inhibited cell apoptosis in hypoxia-induced N2a cells. Moreover, we identified that melatonin can activate the MAPK/ERK pathway via upregulating the expression of Zip1. Therefore, this study provides a new mechanism of melatonin and need our further study in detail. (C) 2015 Elsevier Ireland Ltd. All rights reserved.