• Jing Chen, Guo Zheng, Hu Guo, and Zhong-Nan Shi.
• Department of Neurology, Nanjing Children's Hospital, Nanjing Medical University, No. 72, Guangzhou Road, Gu Lou District, Nanjing, Jiangsu, 210008, People's Republic of China, drchenj@yeah.net.
• J. Mol. Neurosci. 2014 Aug 1;53(4):677-83.

AbstractEndoplasmic reticulum (ER) stress may play a role in status epilepticus (SE). Sprague-Dawley rats were randomized into three groups: control (saline), SE (pentylenetetrazol), and dentate gyrus (DG), pretreated with 2-deoxy-D-glucose (2-DG). Expression levels of glucose-regulated protein 78 (GRP78), CCAAT/enhancer-binding protein homologous protein (CHOP), eukaryotic initiation factor 2α (eIF2α), and protein kinase RNA-like ER kinase (PERK) were determined. CHOP messenger RNA (mRNA) and protein expression levels in SE group were significantly increased as compared to the control group (P < 0.0001), and significantly decreased in DG group as compared to the SE group (P < 0.0001). Phosphorylated eIF-2α protein expression level in SE group was significantly increased as compared to the control group (P < 0.0001) and significantly decreased in DG group as compared to the SE group (P < 0.0001). GRP messenger RNA expression levels and protein levels in SE group was significantly increased as compared to the control group (P < 0.0001) and significantly decreased in DG group as compared to the SE group (P < 0.0001). Phosphorylated PERK protein expression level in SE group was significantly increased as compared to the control group (P < 0.0001), and significantly decreased in DG group as compared to the SE group (P < 0.0001) at the time of 12 and 24 h. Our results suggest that brain injury from SE might involve ER stress via the pro-apoptotic PERK-eIF2α-CHOP signaling pathway.

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