Figure 7.

Schematic graph of the role of ANGPTL8 in TNF‐α‐induced human NP cells ECM catabolism and inflammation. The increased expression of ANGPTL8 was related to ECM degradation and inflammation through enhancing the NF‐κB signalling pathway in TNF‐α‐treated NP cells. Inhibiting of ANGPTL8 partly attenuated the activation of the NF‐κB signalling, and reduced the downstream MMPs and IL‐6 expression. ANGPTL8, angiopoietin‐like protein 8; TNF‐α, tumour necrosis factor α; TNFR, receptor of TNF‐α; NF‐κB, nuclear factor‐kappa B; IKKα, the IκB kinase α; IKKβ, the IκB kinase β; IKKγ, the IκB kinase γ; IκBα, inhibitor of NF‐κB α; IVD, intervertebral disc; NP, nucleus pulposus; ECM, extracellular matrix; MMPs, matrix metalloproteinases; IL‐6, interleukin‐6