Molecular mechanism of activator protein-1 and macrophage inflammatory protein-1α in adjuvant arthritis rats and the effects of sodium arsenite

Objective To study the molecular mechanism of activator protein (AP)-1 and macrophage inflammatory protein (MIP)-1α in adjuvant arthritis and the effects of sodium arsenite (SA) on AP-1 and MIP-1. Methods Forty Wistar female rats were randomly divided into 4 groups: normal control (NC), model (M), low concentration sodium arsenite (SA1) and high concentration sodium arsenite group (SA2). The SA1 group and the SA2 group were treated with sodium arsenite (0.5 mg·kg-1·d-1 and 1.0 mg·kg-1·d-1) through abdominal cavity injection for 20 days, the normal control group and the model group were treated with saline (0.2 ml/d). The levels of C reactive protein (CRP) in every group were determined by biochemistry, the C-fos and MIP-1α expression of synovium in 4 groups were determined by immunohistochemistry. Results The levels of CRP in the M group were increased more than NC group (P0.01), those of the SA1 group and the SA2 group were significantly lower than those of the M group (P0.01). Compared with NC group, the expression of C-fos and MIP-1α in the synovium was up-regulated in the M group (P0.01) and was inhibited by sodium arsenite treatment (P0.05), especially in SA2 group. Conclusion The activated AP-1 and MIP-1α may play an important role in the development of adjuvant arthritis. Sodium arsenite can down-regulate the expression of AP-1 and MIP-1α and may have some therapeutic effects in rheumatiod arthritis (RA).