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目的观察佐剂关节炎(AA)动物模型滑膜组织在诱导凋亡前后的苏木素-伊红(HE)染色及核因子(NF)-κB表达活性的差异,探讨三氧化二砷(As_2O_3)在治疗类风湿关节炎(RA)的可能作用机制。方法将Wistar大鼠造模成功后随机分为两组：AA模型组和As_2O_3治疗组。治疗组每日于发病鼠腹腔注射As_2O_3连续1周,观察3d全部动物处死取材。再经固定、脱钙、包埋,制成切片。然后进行HE染色及免疫组织化学检测。结果HE染色光镜下观察：与正常对照组相比,AA模型组大鼠的滑膜细胞层次增多,6～8层,排列紊乱,有大量炎性细胞浸润；而As_2O_3治疗组可达3～4层,但仍有炎性细胞浸润。免疫组织化学检测结果：AA模型组大鼠关节滑膜的NF-κB(p65)的阳性染色强度明显高于正常对照组,以胞核染色为深,有的成团块状。而As_2O_3治疗组滑膜的NF-κB表达及活性明显下调,但未恢复到正常对照组水平,平均灰度值计算结果显示三组之间差异有统计学意义(P＜0．05)。结论As_2O_3可以抑制分化,诱导滑膜细胞凋亡．而抑制NF-κB的活性和表达可能是As_2O_3发挥治疗作用的重要机制。
Objective To observe the difference of hematoxylin-eosin (HE) staining and nuclear factor (NF) -κB expression in synovial tissue of adjuvant arthritis (AA) animal model before and after induction of apoptosis, and to explore the effect of As 2 O 3 on rheumatoid arthritis The possible mechanism of action of arthritis (RA). Methods Wistar rats were randomly divided into two groups: AA model group and As_2O_3 treatment group. The rats in the treatment group were given intraperitoneal injection of As_2O_3 for 1 week, and all animals were sacrificed. Then fixed, decalcified, embedded, made of slices. Then HE staining and immunohistochemistry were performed. Results Compared with normal control group, the number of synoviocytes in the AA model group increased from 6 to 8 layers, with disordered arrangement and a large number of inflammatory cell infiltration. Compared with the normal control group, the number of synoviocytes in the AA model group was up to 3 ~ Four layers, but still infiltrating inflammatory cells. The results of immunohistochemistry showed that the positive staining intensity of NF-κB (p65) in synovium of AA model group was significantly higher than that of the normal control group, the staining of nucleus was deep, and some became lumps. However, the expression and activity of NF-κB in synovium of As2O3-treated group were significantly down-regulated but not restored to the level in normal control group. The results of mean gray value showed that the difference between the three groups was statistically significant (P <0.05). Conclusion As 2 O 3 can inhibit differentiation and induce synovial cell apoptosis. Inhibition of NF-κB activity and expression may be As_2O_3 play an important role in the treatment of the mechanism.