Attenuating experimental spinal cord injury by hyperbaric oxygen: Stimulating production of vasculoendothelial and glial cell line-derived neurotrophic growth factors and interleukin-10

Po An Tai, Cheng Kuei Chang, Ko Chi Niu, Mao Tsun Lin, Wen Ta Chiu, Chien Min Lin

研究成果: 雜誌貢獻文章

31 引文 (Scopus)

摘要

The present study was carried out to further examine the mechanisms underlying the beneficial effects of hyperbaric oxygen (HBO2) 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. HBO2 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 HBO2 therapy significantly attenuated SCI-induced hindlimb dysfunction, and spinal cord infarction and apoptosis, as well as overproduction of spinal cord interleukin-1β and tumor necrosis factor-α. 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 HBO2. These data suggest that HBO2 may attenuate experimental SCI by stimulating production of GDNF, VEGF, and interleukin-10.
原文英語
頁(從 - 到)1121-1128
頁數8
期刊Journal of Neurotrauma
27
發行號6
DOIs
出版狀態已發佈 - 六月 1 2010

指紋

Glial Cell Line-Derived Neurotrophic Factors
Spinal Cord Injuries
Interleukin-10
Oxygen
Growth
Spinal Cord
Glial Cell Line-Derived Neurotrophic Factor
Laminectomy
Vascular Endothelial Growth Factor A
Hindlimb
Infarction
Apoptosis
DNA Nucleotidylexotransferase
Nerve Growth Factor
Biotin
Interleukin-1
Surgical Instruments
Neuroglia

ASJC Scopus subject areas

  • Clinical Neurology
  • Medicine(all)

引用此文

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title = "Attenuating experimental spinal cord injury by hyperbaric oxygen: Stimulating production of vasculoendothelial and glial cell line-derived neurotrophic growth factors and interleukin-10",
abstract = "The present study was carried out to further examine the mechanisms underlying the beneficial effects of hyperbaric oxygen (HBO2) 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. HBO2 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 HBO2 therapy significantly attenuated SCI-induced hindlimb dysfunction, and spinal cord infarction and apoptosis, as well as overproduction of spinal cord interleukin-1β and tumor necrosis factor-α. 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 HBO2. These data suggest that HBO2 may attenuate experimental SCI by stimulating production of GDNF, VEGF, and interleukin-10.",
keywords = "apoptosis, interleukin-10, neurotrophic factor, spinal cord injury, vascular endothelial growth factor",
author = "Tai, {Po An} and Chang, {Cheng Kuei} and Niu, {Ko Chi} and Lin, {Mao Tsun} and Chiu, {Wen Ta} and Lin, {Chien Min}",
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AU - Niu, Ko Chi

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AB - The present study was carried out to further examine the mechanisms underlying the beneficial effects of hyperbaric oxygen (HBO2) 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. HBO2 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 HBO2 therapy significantly attenuated SCI-induced hindlimb dysfunction, and spinal cord infarction and apoptosis, as well as overproduction of spinal cord interleukin-1β and tumor necrosis factor-α. 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 HBO2. These data suggest that HBO2 may attenuate experimental SCI by stimulating production of GDNF, VEGF, and interleukin-10.

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