Reparative effects of chronic intermittent hypobaric hypoxia pre‑treatment on intervertebral disc degeneration in rats

Abstract

Previous studies have indicated that chronic intermittent hypobaric hypoxia (ciHH) preconditioning can inhibit TnF-α and other related inflammatory cytokines and exerts protective effect on intervertebral disc degeneration disease (idd) in rats; however, the mechanism is still unclear. The present study aimed to explore the repair mechanisms of ciHH on idd in rats. in the experiment, 48 adult Sprague-dawley rats were selected and randomly divided into an experimental group (ciHH-idd), a degenerative group (idd) and a control group (con). The ciHH-idd group of rats (n=16) were treated with ciHH (simulated 3000 m altitude, 5 h per day, 28 days; P o2 =108.8 mmHg) before disc degeneration surgery. The idd group of rats (n=16) underwent tail-vertebral intervertebral disc surgery to establish a model of intervertebral disc degeneration. The con group of rats (n=16) did not receive any treatments. after surgery, the disc height index was calculated using X-ray analysis of rat tail vertebrae, the degeneration process was observed and repair was evaluated by chemically staining degenerative intervertebral disc tissue slices. The expression levels of basic fibroblast growth factor (bFGF), TGFβ1, collagen i and collagen ii were measured in the intervertebral disc tissue using western blotting; while the expression levels of bFGF, TGFβ1 and hypoxia-inducible factor 1-α (HiF-1α) were measured in rat serum using eliSa. The results demonstrated that: i) The degree of intervertebral disc height degeneration in CIHH-IDD rats was significantly lower compared with that in idd rats (P<0.05); ii) the expression levels of bFGF, TGFβ1 and HiF-1α were higher in ciHH-idd rat serum compared with those in idd rat serum (P<0.05); iii) optical microscopy revealed that the degree of disc degeneration was relatively mild in ciHH-idd rats; and iv) the protein expression levels of bFGF, TGFβ1 and collagen ii were increased in ciHH-idd rat intervertebral disc tissues compared with those of idd rats, while the overexpression of collagen i protein was inhibited. overall, after ciHH pre-treatment, the expression levels of bFGF and TGFβ1 were up-regulated, which play notable roles in repairing degenerative intervertebral discs in rats.

Identification of SMIM1 and SEZ6L2 as Potential Biomarkers for Genes Associated with Intervertebral Disc Degeneration in Pyroptosis

“…However, the benefits and drawbacks of the TGF- β signaling pathway for IDD function remain controversial [ 54 ]. Studies have shown that upregulation of TGF β 1 expression can repair degenerated discs and improve the inflammatory response within the disc, protect against degradation of the extracellular matrix, promote cell proliferation, and reduce cell death [ 53 , 55 – 58 ]. Nevertheless, findings in recent years have also shown that over-activation of the TGF- β signaling pathway may accelerate the progression of IDD [ 59 – 61 ].…”

Is Obstructive Sleep Apnea-Associated Adenoid Hypertrophy Linked to Scoliotic Attitudes in Children?

“…Liu et al demonstrated that chronic intermittent hypobaric hypoxia in rats led to increased expression of bFGF, TGFβ1, and HIF-1α. Collagen I and II levels increased, and the nucleus pulposus expanded, constituting over half the disk volume [ 8 ]. Jiang et al reported significant muscle volume and fatty infiltration disparities in adolescent idiopathic scoliosis (AIS) patients, indicating hypoxia's impact on adipose tissue dynamics [ 20 ].…”

“…Recently, there has been increasing recognition of the pivotal role played by hypoxia-inducible factor (HIF) as a crucial molecular component responsible for cellular oxygen sensing and adaptive responses. Furthermore, there have been studies elucidating the production of HIF and structural alterations within the nucleus pulposus when exposed to hypoxic conditions [ 8 ].…”

Pediatric Sleep Questionnaire for Sleep Apnea in Newly Diagnosed Adolescent Idiopathic Scoliosis Patients

“…Studies have indicated that the genetic risk factor significantly amplifies the severity of vertebral defects in combination with brief gestational hypoxia, highlighting the impact of environmental factors [ 11 , 12 ]. Notably, morphological alterations have been observed in the intervertebral disc nucleus pulposus and chondrocytes, showcasing changes under hypoxic conditions [ 13 , 14 , 15 ].…”

“…Prior investigations have elucidated the interconnection among scoliosis, diminished oxygen supply meaning hypoxia, and sleep patterns. Nonetheless, except for the initial assessments of sleep disorders and OSA in scoliosis cases conducted by Mackintosh et al, comprehensive exploration in this realm has been scarce, and other evaluations of OSA have been lacking [ 11 , 12 , 13 , 14 , 15 , 16 , 20 ]. The significance of this relationship persists, insufficiently probed, with a specific dearth of knowledge regarding OSA prevalence.…”