The content of lactic acid gradually increased after annular lesion, associated with the damage of AF structural and the decrease of Col -II and aggrecan in NP tissue, which leading to the disc degeneration.
Our study demonstrated that decreased expression of VDR may play a role in age-related intervertebral disc degeneration in rats and that activation of VDR ameliorates oxidative stress-induced apoptosis in AF cells by preserving mitochondrial functions.
In addition, nucleus pulposus cells stimulated with interleukin-1β (IL-1β) expressed less SIRT3 than that in the control group and nucleus pulposus cells with SIRT3 overexpress vectors expressed more collagen II FOXO3a and superoxide dismutase 2 (SOD2), indicating that SIRT3 could improve the intervertebral disc degeneration by anti-oxidative stress.
The in vivo experiments showed that the HIF-2α controlled the catabolic factors MMP-13 and ADAMTS-4 that regulated the collagen II and aggrecan metabolism in disc degeneration.
Melatonin modulates IL-1β-induced extracellular matrix remodeling in human nucleus pulposus cells and attenuates rat intervertebral disc degeneration and inflammation.
Ligustilide alleviated IL-1β induced apoptosis and extracellular matrix degradation of nucleus pulposus cells and attenuates intervertebral disc degeneration in vivo.
The association of FokI (rs2228570), a polymorphism of the vitamin D receptor gene, with intervertebral disc degeneration (IDD) has been investigated in a multitude of studies.
During intervertebral disc degeneration (IVDD), TNF-α binds to TNF receptors and controls the JNK/ERK-MAPK, and NF-κB signaling pathways in NP cells, increasing CHOP expression.
Animal models of caudal vertebra intervertebral disc degeneration further demonstrated that apoptosis was induced by up-regulation of tumor necrosis factor (TNF) accompanied by down-regulation of NF-κB and MAPKs cascades that are dependent on caspase and RIPK1.
Polymorphisms in several structural and inflammatory genes like collagens, aggrecan, matrix metalloproteinases are associated with the risk of disc degeneration.
We found that serglycin expression increased with increasing disc degeneration both in vivo and in vitro, and also increased with exposure in vitro to IL-1ß and TNF-α.
An in vitro model of disc degeneration using human nucleus pulposus cells (hNPCs) and ex vivo culture of mouse intervertebral discs organs under the actions of inflammatory cytokines were used, and the expression of Col II and aggrecan in hNPCs were detected by semi-quantitative western blot analysis, and the mRNA expression of the genes than encode Col II and aggrecan were detected by reverse transcription‑quantitative polymerase chain reaction (RT-qPCR).
IL-1β and hypoxia synergetically contributed to the catabolic effects of the nucleus pulposus cells by upregulating the expression of MMP-3, MMP-13, ADAMTS-4 and ADAMTS-5 through the activation of NF-κB signaling pathway, indicating that the NF-κB signaling pathway is a key mediator of intervertebral disc degeneration.
Meta-analysis to collect all the relevant studies to further investigate whether or not the FAS ligand (FASL) and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) genetic polymorphisms are associated with susceptibility to intervertebral disc degeneration (IDD) in Chinese Han population.
A systematic review of the relationship between the distributions of aggrecan gene VNTR polymorphism and degenerative disc disease/osteoarthritis.<i>Bone Joint Res</i> 2018;7:308-317.
Sparstolonin B significantly inhibited the IVDD‑induced inflammatory factors tumor necrosis factor‑α, interleukin (IL)‑1β and IL‑6, oxidative stress factors (malondialdehyde), and superoxide dismutase and caspase‑3/9 activities.
The gene expression profiles data were obtained using the same microarray platform for two groups of patients suffering from degenerative disc diseases: GSE41883 (Human annulus disc cells exposed to TNF-a; 4 samples) and GSE27494 (Human annulus disc cells exposed to IL-1β; 4 samples).
Histology and immunostaining revealed that disc degeneration was not significantly different between the OVX + NS rats and the OVX + PTH rats, compared with the Sham group; the structure of nucleus pulposus was disordered, the expression of collagen I was increased, and collagen II and aggrecan were decreased.