中国神经再生研究(英文版)2011,Vol.6Issue(8):635-640,6.DOI:10.3969/j.issn.1673-5374.2011.08.009
Recombinant human erythropoietin for repair of white matter damage
Recombinant human erythropoietin for repair of white matter damage
摘要
Abstract
Erythropoietin has been shown to exhibit neuroprotective effects in animal models. A neonatal rat model of hypoxic-ischemic white matter damage was established via bilateral carotid artery ligation in 4-day-old Sprague-Dawley rats. The rats were subsequently treated with recombinant human erythropoietin to observe pathological changes in the brain and long-term neurobehavioral functions before and after intervention. Results showed that the number of myelin basic protein-positive cells, which reflected myelin/oligodendrocyte damage, significantly increased, although the number of amyloid precursor protein-positive cells, which reflected axonal injury, significantly decreased in periventricular white matter at 72 hours and 7 days following erythropoietin intervention. The number of glial fibrillary acidic protein-positive cells, indicating astrocytic damage, significantly decreased in periventricular white matter of erythropoietin-treated rats at 48 hours, 72 hours, 7 days, and 26 days. Following erythropoietin intervention in the 30-day-old rats, head-turning time in the slope test was shortened and open-field test scores increased. These results suggested that erythropoietin promoted repair of white matter damage, as well as improved neurobehavioral functions in a rat model of hypoxic-ischemic injury.关键词
white matter injury/erythropoietin/neonatal rats/neural behavior/neuroprotectionKey words
white matter injury/erythropoietin/neonatal rats/neural behavior/neuroprotection引用本文复制引用
Wei Zhou,Xiao Rong,Li Tao,Weineng Lu..Recombinant human erythropoietin for repair of white matter damage[J].中国神经再生研究(英文版),2011,6(8):635-640,6.基金项目
This study was financially sponsored by the Natural Science Foundation of Guangdong Prownce,No.5002248 ()
Social Development Science and Technology Project in Guangdong Prownce,No.2006B36030006 ()