首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >Melatonin exerts protective effect on N2a cells under hypoxia conditions through Zip1/ERK pathway
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Melatonin exerts protective effect on N2a cells under hypoxia conditions through Zip1/ERK pathway

机译:褪黑素通过Zip1 / ERK途径对缺氧条件下的N2a细胞发挥保护作用

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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.
机译:褪黑激素在不同的中枢神经系统损伤中起神经保护作用。然而,尚不清楚褪黑激素对神经保护的分子机制。在这里,我们研究了褪黑素在缺氧诱导的N2a细胞中的作用,我们的结果表明褪黑素不仅降低了ROS和MDA的水平,诱导了SOD的增加,而且还增加了缺氧诱导的N2a细胞的增殖和抑制细胞凋亡。 N2a细胞。此外,我们发现褪黑激素可以通过上调Zip1的表达激活MAPK / ERK途径。因此,本研究提供了褪黑激素的新机制,需要我们进一步深入研究。 (C)2015 Elsevier Ireland Ltd.保留所有权利。

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