川芎嗪对类风湿性关节炎外周血RANK／RANKL／骨保护素途径干预作用的研究

目的观察川芎嗪对类风湿性关节炎（RA）模型大鼠RANK／RANKL／0PG在外周血中CD3^＋T淋巴细胞、中性粒细胞、CD14单核细胞的表达率及平均荧光强度，探讨川芎嗪在RA骨破坏和炎症过程巾的意义。方法大鼠随机分成5组，正常对照组、模型对照组、川芎嗪大剂量组、川芎嗪小剂量组、阳性药物对照组，每组10只。给药7d后，应用间接免疫荧光标记和流式细胞技术对各组大鼠外周血相关指标进行检测分析。结果与正常对照组相比，RA大鼠骨保护素（OPG）表达明显降低，从正常的24．7降至18．7（q=4．2，P〈0．05），RANK、RANKL变化不明显，经过川芎嗪治疗后，大剂量组OPG有明显的回升，至23．8％（q=3．97，P〈0．05），小剂量组变化不明显。RANK在CD3^＋细胞、中性粒细胞、CD14单核细胞上的平均荧光强度明显降低，分别为20．6、135．4、84．2，经川芎嗪大剂量治疗后明显升高，分别达到31．0、192．1、95．6（q=10．4、q=8．6、q=6．3，P〈0．05）。结论大剂量川芎嗪可以通过调节OPG／RANK／RANKL途径对RA起一定的作用。

Intervention effects of Ligustrazine on the RANK/RANKL/Osteoprotegerin pathway in peripheral blood of Rheumatoid Arthritis

Objective To observe the expression rate and the average fluorescence intensity of receptor activator of NF-kB (RANK), RANK ligand (RANKL) , Osteoprotegerin (OPG) of CD3~+ T lymphocytes, neu-trophils, and CD14 monocyte in the peripheral blood of rheumatoid arthritis (RA) model rats and to explore the significance of bone destruction and inflammation in the process of RA by using Ligustrazine. Methods Rats were randomly divided into five groups, the normal group, the model control group, high dosage Ligustrazine group, low dosage Ligustrazine group and positive drug group. Each group had ten animals. After 7 days, peripheral blood of rats was examined by indirect immunofluorescence and flow cytometry technology. Results The OPG expression was decreased significantly from 24.7% to 18.7% compared with the control group (q=4.2, P<0.05) and increased to 23. 8%(g=3.97, P<0.05) after high-dose Ligustrazine treatment, but the expression of RANK and RANKL did not change significantly in RA rats treated with high-dose and low-dose ligustrazine group. The average fluorescence intensity of RANK in CD3~+ T cells, neutrophils, and CD14 monocytes in RA rats decreased significantly to 20.6, 135.4 and 84.2, respectively, but increased after high-dose ligustrazine treatment to 31.0, 192.1 and 95.6 (q = 10. 4, q =8. 6, q=6.3, P<0.05). Conclusion High-dose ligustrazine plays a role on RA by regulating the RANK/RANKL/ OPG pathway.