<b>Conclusion:</b> The expression level of various proteolytic enzymes such as aminopeptidase in the intervertebral disc and the linear relationship between microvessel formation and nerve fiber ingrowth in the intervertebral disc are helpful to further explore the molecular level of disc degeneration and pathophysiological mechanisms to aid clinical diagnosis and treatment of such diseases.
In addition, we showed that miR-203 expression was downregulated in degenerative NP samples, and miR-203 expression reduced gradually along with the grade of exacerbation of disc degeneration.
We showed that the expression of lncRNA LINC00958 was upregulated in degenerative NP samples, and LINC00958 expression increased gradually along with the grade of exacerbation of disc degeneration.
LAMP2 rose with increasing disc degeneration grade through grade V. In the quantitative analysis of colocalization, grade III is significantly higher than grade II and V (P < 0.05).
The mechanisms of intervertebral disc degeneration include changes in extracellular matrix (ECM) deposition and tissue fibrosis. sIL-13Rα2-Fc potently inhibits interleukin (IL)-13, as well as blocks related cell signaling pathways and inhibits fibrosis in certain tissues.
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.
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.
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.
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.
Melatonin modulates IL-1β-induced extracellular matrix remodeling in human nucleus pulposus cells and attenuates rat intervertebral disc degeneration and inflammation.
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.