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沉默编码 C/EBP 同源蛋白的基因可减轻缺血/再灌注后的急性脑损伤。

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

机构信息

Department of Neurology, Bethune First Hospital, Jilin University, Changchun 130021, Jilin Province, China.

Department of Neonatology, Bethune First Hospital, Jilin University, Changchun 130021, Jilin Province, China.

出版信息

Neural Regen Res. 2012 Nov 5;7(31):2432-8. doi: 10.3969/j.issn.1673-5374.2012.31.004.

DOI:10.3969/j.issn.1673-5374.2012.31.004
PMID:25337093
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4200717/
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.

摘要

C/EBP 同源蛋白是内质网应激过程中的一种重要转录因子，参与内质网应激介导的细胞凋亡。既往研究表明，C/EBP 同源蛋白在阿尔茨海默病、蛛网膜下腔出血和脊髓创伤中介导神经损伤。在这项研究中，我们通过左侧侧脑室注射慢病毒载体将 C/EBP 同源蛋白短发夹 RNA 导入脑缺血/再灌注大鼠模型。沉默 C/EBP 同源蛋白基因表达可显著减少脑梗死体积，降低脑梗死组织中肿瘤坏死因子-α和白细胞介素-1βmRNA 表达，减少梗死区域 TUNEL 阳性细胞数，降低半胱氨酸天冬氨酸蛋白酶-3 蛋白含量，增加 B 细胞淋巴瘤-2 蛋白含量。这些结果表明，沉默 C/EBP 同源蛋白可减少细胞凋亡和炎症反应，从而起到神经保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3be6/4200717/facfba31478b/NRR-7-2432-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3be6/4200717/53674fd2afe2/NRR-7-2432-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3be6/4200717/b19e56ebebdb/NRR-7-2432-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3be6/4200717/b6a5126c247f/NRR-7-2432-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3be6/4200717/facfba31478b/NRR-7-2432-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3be6/4200717/53674fd2afe2/NRR-7-2432-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3be6/4200717/b19e56ebebdb/NRR-7-2432-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3be6/4200717/b6a5126c247f/NRR-7-2432-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3be6/4200717/facfba31478b/NRR-7-2432-g004.jpg

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