Melatonin exerts protective effect on N2a cells under hypoxia conditions through Zip1/ERK pathway

被引：16

作者：

Liu, Xin-Wei ^{[1
]}

Zi, Ying ^{[2
]}

Liu, Yun-En ^{[3
]}

Zhang, Yu-Biao ^{[3
]}

Xiang, Liang-Bi ^{[1
]}

Hou, Ming-xiao ^{[3
]}

机构：

[1] Gen Hosp Shenyang Mil Area Command Chinese PLA, Dept Orthoped, Rescue Ctr Severe Wound & Trauma PLA, Shenyang 110016, Liaoning Provin, Peoples R China

[2] 463rd Hosp PLA, Dept Emergency, Shenyang 110042, Liaoning Provin, Peoples R China

[3] Gen Hosp Shenyang Mil Area Command PLA, Lab Severe & War Related Trauma Ctr, Shenyang 110016, Liaoning Provin, Peoples R China

来源：

NEUROSCIENCE LETTERS | 2015年 / 595卷

关键词：

Melatonin; N2a cells; Zip1; ERK1/2; ERK5; Apoptosis; OXIDATIVE STRESS; THYROID-HORMONES; ZINC; RATS; APOPTOSIS; ACTIVATION; EXPRESSION; CHANNELS; ENZYMES; DEATH;

D O I：

10.1016/j.neulet.2015.04.013

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

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.

引用

页码：74 / 80

页数：7

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