TNFAIP3 alleviates pain in lumbar disc herniation rats by inhibiting the NF-κB pathway

It's been reported that the tumor necrosis factor alpha inducible protein 3 (TNFAIP3) gene played an important role in the pathogenesis of autoimmune and chronic inflammation diseases. Moreover, in degenerative diseases of the lumbar spine the nuclear factor-κB (NF-κB) pathway is significantly activated. This study aimed to explore the role of the tumor necrosis protein-induced zinc finger protein A20 (A20) protein in degenerative diseases of the lumbar spine on the NF-κBp65 pathway.

A total of 96 rats were randomly divided into 4 groups. Lumbar disc herniation (DH) was set as a sham operation group (Sham group), DH + A20 group and DH + control group (Control group); measured changes in rat paw withdrawal threshold (PWT) and paw withdrawal latency (PWL); detected the proportion of apoptotic cells in a single nucleus pulposus cell suspension, analyzed the correlation between tumor necrosis factor-α (TNF-α) content and pain in DH rats, and the expression changes of NF-κB pathway in nucleus pulposus tissue.

compared with the DH + Control group, the PWT and PWL of the DH + A20 group increased significantly (P<0.05); apoptosis in the DH + A20 group was significantly reduced (P<0.01); the nucleus pulposus tissue and serum levels of TNF-α and interleukin-6 (IL-6) in the DH + A20 rat group were significantly lower than those in the DH + Control group (P<0.05); the protein expression of rats in the DH + A20 group (p-p65) was significantly lower than that in the DH + Control group (P<0.05).

The pain of lumbar disc herniation rats is related to TNF-α, and overexpression of A20 protein can reduce the pain of lumbar disc herniation by inhibiting the NF-κB pathway.

Lumbar disc herniation (lumbar DH); tumor necrosis factor-α (TNF-α); interleukin-6 (IL-6); tumor necrosis factor alpha inducible protein 3 (TNFAIP3).