| Inflammation is one of the major causes that contribute to intervertebral disc degeneration(IDD).Emerging evidence have revealed that increased pro-inflammatory cytokines such as interleukin 6(IL-6)and tumor necrosis factor alpha(TNF-α)can trigger a variety of signaling pathways,eventually resulting IDD.Here,we show that two cullin members CUL4 A and 4B,but not other cullin members,are specifically overexprssed in IDD samples,and positively correlated with the severity of IDD,In the in vitro cytology test,the treatment of IL-6 and TNF-α can significantly down-regulate mi R-194-5p,thereby inducing a significant increase in the expression levels of CUL4 A and 4B,leading to inflammatory reactions in cells.Metformin prevents the release of HMGB1 from the nucleus into the cytoplasm,thereby reducing the protein activity of senescence-associated β-gal and the expression of TNF-α,IL-1β,IL-6,MMP-3 and MMP-13 genes,thereby inhibiting intervertebral disc cells.Aging and inflammation occur.At the same time,in clinical practice,ACDF has become a classic surgical procedure for cervical spondylosis caused by degeneration of the intervertebral disc,and the appearance of the plate screw fixation system strengthens the stability of the cervical spine after surgery and reduces the failure of fusion.The formation of the pseudo joint caused.However,the stress shielding of the rigid steel plate causes the sedimentation of the implant or the bone block,and the complications of screw extraction and fracture are also receiving more and more attention.The sliding steel plate can well solve the stress shielding of the rigid steel plate,thereby achieving a better therapeutic effect.In conclusion,these findings provide new ideas and directions for studying the pathogenesis of inflammation leading to degeneration of the intervertebral disc,and provide new treatments and methods for clinical prevention or treatment of IDD. |
