Neural Regeneration Research ›› 2012, Vol. 7 ›› Issue (31): 2432-2438.

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Silencing the gene encoding C/EBP homologous protein lessens acute brain injury following ischemia/reperfusion

Fengzhang Wang1, Yuan Zhang2, Chunke He3, Tingting Wang4, Qiyan Piao5, Qun Liu1   

  1. 1 Department of Neurology, Bethune First Hospital, Jilin University, Changchun 130021, Jilin Province, China
    2 Department of Neonatology, Bethune First Hospital, Jilin University, Changchun 130021, Jilin Province, China
    3 Department of Orthopedics, Jilin Hospital of Integrated Traditional and Western Medicine, Changchun 130021, Jilin Province, China
    4 Department of Infectious Diseases, Zibo First Hospital, Zibo 255200, Shandong Province, China
    5 Department of Cardiology, General Hospital of China National Petroleum Corporation in Jilin, Jilin 132021, Jilin Province, China
  • Received:2012-07-23 Revised:2012-10-31 Online:2012-11-05 Published:2012-11-05
  • Contact: Qun Liu, M.D., Chief physician,Department of Neurology,Bethune First Hospital, Jilin University, Changchun 130021,Jilin Province, China songleisl@163.com
  • About author:Fengzhang Wang☆, M.D.,Chief physician, Department of Neurology, Bethune First Hospital, Jilin University,Changchun 130021, Jilin Province, China

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Abstract:

C/EBP homologous protein, an important transcription factor during endoplasmic reticulum stress,participates in cell apoptosis mediated by endoplasmic reticulum stress. Previous studies have shown that C/EBP homologous protein mediates nerve injury during Alzheimer’s disease,subarachnoid hemorrhage and spinal cord trauma. In this study, we introduced C/EBP homologous protein short hairpin RNA into the brains of ischemia/reperfusion rat models via injection of lentiviral vector through the left lateral ventricle. Silencing C/EBP homologous protein gene expression significantly reduced cerebral infarction volume, decreased water content and tumor necrosis factor-α and interleukin-1β mRNA expression in brain tissues following infarction, diminished the number of TUNEL-positive cells in the infarct region, decreased caspase-3 protein content and increased Bcl-2 protein content. These results suggest that silencing C/EBP homologous protein lessens cell apoptosis and inflammatory reactions, thereby protecting nerves.

Key words: C/EBP homologous protein, endoplasmic reticulum stress, Alzheimer’s disease, subarachnoid hemorrhage, tumor necrosis factor-α;ischemia/reperfusion;interleukin-1β, cerebral infarction;neural regeneration