RANKL在佐剂性关节炎大鼠滑膜中的表达及亚砷酸对其影响

Expression of recept activator of nuclear factor-κB ligand (RANKL) of synovium in adjuvant arthritis rats and effects of sodium arsenite on them

目的:研究细胞核因子-κB受体活化因子配基(receptor activator of nuclear factor-κB ligand,RANKL)在佐剂性关节炎大鼠发病中的作用,探讨亚砷酸对RANKL的影响及其对佐剂性关节炎大鼠的治疗作用。方法:40只大鼠随机分成4组:正常对照组、模型组、低剂量亚砷酸组(LSA,1.5 mg.kg-1.d-1)、高剂量亚砷酸组(HSA,3.0 mg.kg-1.d-1),正常对照组与模型组给予生理盐水2 ml/d。免疫组化、原位杂交方法检测各组RANKL蛋白及其mRNA的表达;HE染色观察各组滑膜组织形态变化。结果:与正常对照组比较,模型组RANKL蛋白及其mRNA大量表达(P<0.01);与模型组比较,LSA组及HSA组RANKL蛋白及其mRNA表达降低(P<0.01),且HSA组更明显。结论:RANKL在大鼠佐剂性关节炎发生发展中具有重要作用;亚砷酸能下调RANKL蛋白及其mRNA的表达,提示亚砷酸对RA有一定的治疗作用。

Objective：To study the expression of receptor activator of nuclear factor-kB ligand（RANKL） in synovium of adjuvant arthritis rats and effects of sodium arsenite（SA）on RANKL. Methods：Forty Wistar female rats were randomly divided into 4 groups ： normal control group, model group, low concentration sodium arsenite group （LSA） and high concentration sodium arsenite group（HSA）. LSA group and HAS group were treated with SA（ 1.5 mg· kg^-1· d^-1 and 3 mg ·kg^-1· d^-1 ）through abdominal injection, the normal control group and the model group were treated with saline（ 1 ml/d）. The expressions of RANKL protein and mRNA of synovium by immunohistochemistry and by in situ hybridization. Light microscope was used to observe the synovium by HE. Results ： Compared with normal control group, the expressions of RANKL protein and mRNA in the synovium were up-regulated in the model group （P 〈 0. 01 ） and were inhibited by sodium arsenite （P 〈 0. 01 ）, especially in the HAS group. Conclusion： RANKL may play an important role in the development adjuvant arthritis. Sodium arsenite can down-regulate the expressions of RANKL protein and mRNA and may have some therapeutic effects in rheumatoid arthritis.