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 (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.

Hyperbaric oxygen therapy for spinal cord ischaemia after complex aortic repair — a retrospective review

“…Rats with compression spinal cord injury treated with HBOT immediately after the insult had smaller spinal cord infarction, less apoptosis, decreased spinal cord production of interleukin-1beta and tumour necrosis factor-alpha, lower expression of HIF-1alpha and higher production of interleukin-10 and vasculo-endothelial and glial cell line-derived neurotrophic growth factors in comparison with untreated controls [18][19][20]. These findings correlated with the better motor function scores in the HBOT treated animals [18,19].…”

Hyperbaric oxygen therapy of spinal cord injury

“…Many studies have used terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling (TUNEL) staining to show that HBO therapy significantly reduces apoptosis in injured spinal cord tissue, and most of the studies have proposed potential pathways by which HBO therapy attenuates apoptotic cell death after SCI 1519202327303133…”

Hyperbaric Oxygen Therapy in Acute Ischemic Stroke: A Review

“…Numerous studies have shown that HBO significantly improves the levels of BDNF, GDNF and NGF in ischemic injury. Simultaneously, studies have shown that the positive effects still exist in brain damage [75] and spinal cord injury [76] . Long-course and repeated HBO therapy for cerebral ischemia can also generate similar outcomes [52,77] .…”