Relationship between serum inflammatory cytokine levels and NF-κB expression in rat synovial cells

Rheumatoid arthritis (RA) is a type of autoimmune disease caused by cytokines eroding articular synovium induced inflammation. NF-kappa B plays a role of switching cell activity in cells. It was suggested that NF-kappa B participates in inflammatory response, promotes cell apoptosis, and leads to cell cycle differentiation. It is the main pathological factor of RA. This paper studies the correlation relationship between CIA rats arthritis with NF-kappa B and IL-17. A total of 80 SD rats were randomly divided as control and model group. CIA rat model was established in model group. Toe volume and arthritis index (AI) were applied to evaluate joint inflammation. IL-17 level was detected by enzyme-linked immunosorbent method (ELISA). NF-kappa B/P65, NF-kappa B/P50, and I kappa Ba expression in synovial cells were tested by western blot. Compared with blank control, the toe volume in model rat was similar in the 1st day and 5th day (P>0.05). The toe volume significantly increased at 10th, 15th, and 20th day after modeling compared with control (P<0.05). AI showed no statistical difference in the 5th and 10th day after modeling compared with control (P>0.01). AI elevated markedly at 15th and 20th day after modeling (P<0.01). IL-17 significantly increased in model group compared with control (P<0.01). NF-kappa B/P65, NF-kappa B/P50, and I kappa B alpha expression obviously enhanced in model group compared with control (P<0.01). NF-kappa B highly expression in CIA rat model synovial cells was related to IL-17 highly expression.