The in vivo results showed that TLR4 and p-p65 proteins were highly expressed in IVD tissues of IDD rats, and PU intervention could downregulate their expression, suggesting that the TLR4/NF-κB pathway was involved in the pathogenesis of IDD and may be related to the mechanism of PU intervention in IDD. Here, NFKB1 is linked to intervertebral disk degenerative disorder.