NGF protects against oxygen and glucose deprivation-induced oxidative stress and apoptosis by up-regulation of HO-1 through MEK/ERK pathway. (22nd February 2017)

• Record Type: Journal Article
• Authors: Sun, Zhitang; Hu, Weimin; Yin, Shulan; Lu, Xiufang; Zuo, Wenchao; Ge, Sihui; Xu, Yuming
• Is Part Of: Neuroscience letters. Volume 641(2017)
• Page Start: 8
• Page End: 14
• Publication Date: 2017-02-22
• Subjects: NGF -- HO-1 -- OGD -- ERK -- Neuroprotection -- ROS -- Apoptosis; Neurology -- Periodicals; Neurology -- Periodicals; Research -- Periodicals; Neurologie -- Périodiques; Neuroanatomie -- Périodiques; Neuropharmacologie -- Périodiques; Neurophysiologie -- Périodiques; Neurology; Periodicals; Electronic journals; 617.48
• DOI: 10.1016/j.neulet.2017.01.046
• Languages: English
• ISSNs: 0304-3940

Abstract

Highlights: NGF induces expression of HO-1 in primary cultured cortical neurons, it confers neuroprotection effect on OGD insult. NGF activates ERK1/2 phosphorylation. The MEK/ERK pathway is involved in NGF-induced HO-1 expression, and neuroprotection. Cell death was controlled by MEK/ERK survival pathway at least partly through inducing the expression of HO-1. Abstract: 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.