Abstract

An in vivo study was conducted to test the effect of hyperbaric oxygenation (HBO) on intervertebral disc degeneration in Sprague-Dawley rats. To observe the changes in intervertebral disc height and levels of glycosaminoglycan, collagen, interleukin-1β (IL-1β), prostaglandin E2 (PGE2), and inducible nitric oxide synthase (iNOS) in degenerated intervertebral discs after HBO therapy. Although the involvement of IL-1β, PGE-2, NO, and low O2 concentration has been demonstrated in intervertebral disc degeneration, the actual mechanism is not clear. It has been reported that HBO influences changes in IL-1β, PGE-2, NO, and O2 concentration. Previously, a study demonstrated an in vitro positive effect of HBO on the human nucleus pulposus. Thus, an in vivo study in animals was necessary. Twelve Sprague-Dawley rats were each injected with chondroitinase ABC in 2 proximal intervertebral discs of the tail. After treating with 100% oxygen at 2.5 atmospheres 2 hours per days for 10 days, the change in disc height was determined by radiography. The amounts of PGE-2, iNOS, glycosaminoglycan, and total collagen in the intervertebral disc were quantified by enzyme-linked immunosorbent assay. Tissue morphology and the distribution of glycosaminoglycan, IL-1β, and iNOS in the intervertebral disc were assessed by histology and immunohistochemistry. The area of IL-1β in the intervertebral discs was quantified using image analysis software. HBO therapy stopped the decrease in intervertebral disc height, caused an increase in the amount of glycosaminoglycan, and inhibited IL-1β, PGE-2, and iNOS production. HBO provides a potential treatment modality for intervertebral disc degeneration.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.