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Erythropoietin Markedly Attenuates Brain Infarct Size and Improves Neurological Function in the Rat

Authors :
Hon-Kan Yip
Han-Tan Chai
Fan-Yen Lee
Steve Leu
Sheung-Fat Ko
Yu-Chun Lin
Sarah Chua
Chun-Man Yuen
Cheuk-Kwan Sun
Chia-Hung Yen
Jiunn-Jye Sheu
Sheng-Ying Chung
Source :
Journal of Investigative Medicine. 58:893-904
Publication Year :
2010
Publisher :
SAGE Publications, 2010.

Abstract

Background The impact of epoetin beta (recombinant human erythropoietin) on brain infarction area (BIA) and neurological status in a rat model of acute ischemic stroke (IS) induced by distal left internal carotid artery occlusion was investigated. Methods Adult male Sprague-Dawley rats (n = 30) were categorized into group 2 (IS only) and group 3 (IS plus intraperitoneal erythropoietin 5000 IU/kg at 0, 12, and 24 hours after IS). Healthy Sprague-Dawley rats (n = 10) served as group 1. Results Analysis of brain tissues showed larger BIA in group 2 than in group 3 ( P < 0.001). Corner test identified highest frequency of left turn in group 2 ( P < 0.05). The mRNA expressions of Bax, caspase 3, interleukin 18, toll-like receptor 4, and plasminogen activator inhibitor 1 were highest, whereas Bcl-2 was lowest in group 2 ( P < 0.05). Lower CXCR4 and stromal cell-derived factor 1 expressions were noted in group 2 than in group 3 ( P < 0.01). Immunohistofluorescence staining showed lower expressions of CXCR4, stromal cell-derived factor 1, von Willebrand factor, and doublecortin with higher number of apoptotic nuclei in group 2 than in group 3 ( P < 0.001). Immunohistochemical staining demonstrated lower cellular proliferation and number of small vessels with higher glial fibrillary acid protein expression in group 2 than in group 3 ( P < 0.01). Conclusions Erythropoietin significantly limited BIA and improved sensorimotor dysfunction after acute IS.

Details

ISSN :
17088267 and 10815589
Volume :
58
Database :
OpenAIRE
Journal :
Journal of Investigative Medicine
Accession number :
edsair.doi.dedup.....60d68e26422dcb9f57c1ecd1a81188f2