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

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.

• Authors: Fengzhang Wang, Yuan Zhang, Chunke He, Tingting Wang, Qiyan Piao, Qun Liu
• Journal: Neural regeneration research (Neural Regen Res) Vol. 7 Issue 31 Pg. 2432-8 (Nov 05 2012) ISSN: 1673-5374 [Print] India
• PMID: 25337093 (Publication Type: Journal Article)