Abstract:

BACKGROUND: Previous research has demonstrated that multiple cytokines and inflammatory transmitters participate in pathopoiesis of rheumatoid arthritis. Thalidomide was an immunomodulator which used to treat rheumatoid disease.

OBJECTIVE: To study the effect of thalidomide on inflammatory arthropathy and tumor necrosis factor-alpha (TNF-α) expression in a rat model of collagen induced arthritis (CIA).

METHODS: Wistar rats were randomly divided into 4 groups. All rats except the normal group were intradermally injected with the emulsion of type II collagen and complete Freund's adjuvant to induce arthritis model. After 10 days, rats of normal group and model group were given an intragastric administration with distilled water, rats of thalidomide group were given an intragastric administration with thalidomide, and rats of methotrexate (MTX) group were given an intragastric administration with MTX. The thickness of the claws and the concentration of TNF-α were measured or detected before and at 7, 14, 21, 28, 35, 42, and 60 days after operation, and the pathological score and radiography of ankle joint were evaluated.

RESULTS AND CONCLUSION: Thalidomide effectively relieved swelling of ankle joint of CIA rats. On the 28^th day, the thickness of the claws of the model group was significantly greater than of thalidomide group (P < 0.05). To compare with model group, the concentration of TNF-α in blood plasma decreased after 14 days in thalidomide group (P < 0.05). The pathological scores of the thalidomide group were significantly less than of model group between 14 and 60 days. The time of osteoclasia in thalidomide group was later than of model group (P < 0.01), and the degree of osteoclasia was milder. There was no significant difference between thalidomide and MTX groups. Thalidomide can effectively lighten disease progression in the CIA rats through influencing TNF-α expression and suppressing synovitis and histoclasia in the joint.