Document Detail


Attenuating experimental spinal cord injury by hyperbaric oxygen: stimulating production of vasculoendothelial and glial cell line-derived neurotrophic growth factors and interleukin-10.
MedLine Citation:
PMID:  20334467     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The present study was carried out to further examine the mechanisms underlying the beneficial effects of hyperbaric oxygen (HBO(2)) on experimental spinal cord injury (SCI). Rats were divided into three major groups: (1) sham operation (laminectomy only); (2) laminectomy + SCI + normobaric air (NBA; 21% oxygen at 1 ATA); and (3) laminectomy + SCI + HBO(2) (100% oxygen at 2.5 ATA for 2 h). Spinal cord injury was induced by compressing the spinal cord for 1 min with an aneurysm clip calibrated to a closing pressure of 55 g. HBO(2) therapy was begun immediately after SCI. Behavioral tests of hindlimb motor function as measured by the Basso, Beattie, and Bresnahan (BBB) locomotor scale was conducted on days 1-7 post-SCI. The triphenyltetrazolium chloride staining assay and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate biotin nick-end labeling assay were also conducted after SCI to evaluate spinal cord infarction and apoptosis, respectively. Cells positive for glial cell line-derived neurotrophic nerve growth factor (GDNF) and vascular endothelial growth factor (VEGF) and cytokines in the injured spinal cord were assayed by immunofluorescence and commercial kits, respectively. It was found that HBO(2) therapy significantly attenuated SCI-induced hindlimb dysfunction, and spinal cord infarction and apoptosis, as well as overproduction of spinal cord interleukin-1beta and tumor necrosis factor-alpha. In contrast, the numbers of both GDNF-positive and VEGF-positive cells and production of spinal cord interleukin-10 after SCI were all significantly increased by HBO(2). These data suggest that HBO(2) may attenuate experimental SCI by stimulating production of GDNF, VEGF, and interleukin-10.
Authors:
Po-An Tai; Chen-Kuei Chang; Ko-Chi Niu; Mao-Tsun Lin; Wen-Ta Chiu; Chien-Min Lin
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of neurotrauma     Volume:  27     ISSN:  1557-9042     ISO Abbreviation:  J. Neurotrauma     Publication Date:  2010 Jun 
Date Detail:
Created Date:  2010-06-21     Completed Date:  2010-09-22     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8811626     Medline TA:  J Neurotrauma     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1121-7     Citation Subset:  IM    
Affiliation:
Graduate Institute of Clinical Medicine, Taipei Medical University, Taipei, Taiwan.
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MeSH Terms
Descriptor/Qualifier:
Analysis of Variance
Animals
Apoptosis / physiology
Cell Count
Glial Cell Line-Derived Neurotrophic Factor / metabolism*
Hindlimb / physiopathology
Hyperbaric Oxygenation*
Interleukin-10 / metabolism*
Laminectomy
Male
Motor Activity
Random Allocation
Rats
Rats, Sprague-Dawley
Spinal Cord / metabolism*
Spinal Cord Injuries / metabolism,  physiopathology,  therapy*
Vascular Endothelial Growth Factor A / metabolism*
Chemical
Reg. No./Substance:
0/Glial Cell Line-Derived Neurotrophic Factor; 0/Vascular Endothelial Growth Factor A; 130068-27-8/Interleukin-10

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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