亚砷酸对类风湿性关节炎大鼠治疗作用的研究

目的： 探讨类风湿性关节炎大鼠发病机制并观察亚砷酸对AP-1和MIP-1α表达的影响。方法：随机将32只大鼠分成4组:对照组(C组)、关节炎组（A组）、LSA组（腹腔注射亚砷酸0.5 mg·kg^-1·d^-1）、HSA组（腹腔注射亚砷酸1.0 mg·kg^-1·d^-1）。免疫组织化学检测各组AP-1、MIP-1α表达；采用HE法观察滑膜病理改变。结果： C组未见AP-1和MIP-1α表达，A组AP-1及MIP-1α表达明显高于C组（P<0.05）； LSA组及HSA组AP-1、MIP-1α表达低于A组（P<0.05），且HSA组更明显。结论： AP-1和MIP-1α可能参与大鼠佐剂性关节炎发生、发展；亚砷酸能下调AP-1和MIP-1α表达,可能对RA有一定治疗作用。

Therapeutic effect of sodium arsenite on rheumatoid arthritis in rats

AIM:To study the molecular mechanism of rheumatoid arthritis (RA) and the effects of sodium arsenite on AP-1 and MIP-1. METHODS:32 Wistar female rats were randomly divided into 4 groups: normal control (C), arthritis (A), low concentration of sodium arsenite (LSA) and high concentration of sodium arsenite group (HSA).The LSA group and the HSA 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 AP-1 and MIP-1α expression of synovium in four groups were determined by immunohistochemistry. Light microscope was used to observe the synovium with HE staining. RESULTS:Compared with C group, the expression of AP-1 and MIP-1α in the synovium up-regulated in A group (P<0.01) and were inhibited by sodium arsenite treatment (P<0.05), especially in HSA group. CONCLUSION:The activated AP-1 and MIP-1α play an important role in the development of rheumatoid arthritis. Sodium arsenite down-regulated the expression of AP-1 and MIP-1α and may have some therapeutic effects in RA.