NGF protects against oxygen and glucose deprivation-induced oxidative stress and apoptosis by up-regulation of HO-1 through MEK/ERK, pathway

被引:30
作者
Sun, Zhitang [1 ,2 ]
Hu, Weimin [2 ]
Yin, Shulan [2 ]
Lu, Xiufang [2 ]
Zuo, Wenchao [2 ]
Ge, Sihui [2 ]
Xu, Yuming [1 ]
机构
[1] Zhengzhou Univ, Affiliated Hosp 1, Dept Neurol, Zhengzhou 450052, Henan, Peoples R China
[2] Shanxi Med Univ, Dept Neurol, Hosp 2, 382 Wuyi Rd, Taiyuan 030001, Shanxi, Peoples R China
基金
中国国家自然科学基金;
关键词
NGF; HO-1; OGD; ERK; Neuroprotection; ROS; Apoptosis; MESENCHYMAL STEM-CELLS; CEREBRAL-ISCHEMIA; INJURY; NEUROPROTECTION; REPERFUSION; NEURONS; NRF2; ACTIVATION; DAMAGE; ERK1/2;
D O I
10.1016/j.neulet.2017.01.046
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Both nerve growth factor (NGF) and heme oxygenases-1 (HO-1) promotes neuron survival from cerebral ischemic lesions. NGF protects neurons from oxygen-glucose deprivation (OGD), and HO-1 expression can be induced by some growth factors like NGF. This work attempted to identify the contribution of HO-1 on the neuroprotection role of NGF in OGD model, which is an injury simulation of ischemic neuron in vitro. The viability of cortical neurons cells treated with OGD restored significantly by pretreatment with NGF in a dose dependent manner. Moreover, NGF provided obvious protective effects against OGD-induced neurons apoptosis. It identified that NGF could prevent apoptosis and ROS (reactive oxygen species) accumulation in the primary cortical neurons exposed to OGD. NGF could up-regulate the expression level of HO-1, and then afford neuroprotection against OGD insult. In addition, we found that MEK/ERK pathway participated NGF-induced over-expression of HO-1, and was involved in the transcriptional activity or neuroprotection effect of NGF. (C) 2017 Published by Elsevier Ireland Ltd.
引用
收藏
页码:8 / 14
页数:7
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