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目的:观察补肾抗风湿方药寒痹康汤对CIA大鼠骨组织RANKL/RANK/OPG系统的影响,揭示其抗类风湿关节炎骨质侵蚀的作用机制。方法:采用弗氏不完全佐剂乳化的牛Ⅱ型胶原蛋白诱导CIA大鼠模型,将60只Wistar大鼠随机分为正常对照组,模型对照组,甲氨蝶呤组,寒痹康汤高、中、低剂量组,以甲氨蝶呤组为对照,观察不同剂量寒痹康汤对CIA大鼠骨组织RANKL、RANK和OPG表达水平的影响。结果:与正常对照组比较,模型对照组大鼠骨组织的RANKL m RNA、RANK m RNA、RANKL蛋白、RANK蛋白的表达升高,OPG m RNA、OPG蛋白的表达下降(P<0.01);与模型对照组比较,寒痹康汤各剂量组和甲氨蝶呤组的RANKL m RNA、RANK m RNA、RANKL蛋白、RANK蛋白的表达均有不同程度的下降,OPG m RNA、OPG蛋白的表达均有不同程度的升高(P<0.01或P<0.05),其中以寒痹康汤高剂量组最明显;寒痹康汤高剂量组与甲氨蝶呤组比较,差异无统计学意义(P>0.05)。结论:寒痹康汤能抑制CIA大鼠的关节炎严重度,提高骨组织中OPG蛋白和基因表达,抑制RANKL和RANK的蛋白和基因表达,提示其具有抗类风湿关节炎骨质侵蚀的作用,机制可能与调控OPG/RANKL/RANK破骨细胞分化调节信号传导系统有关。
Objective: To observe the effect of Bushen anti-rheumatism recipe Hanbi Decoction on RANKL / RANK / OPG system in bone of CIA rats, and to reveal its mechanism of anti-rheumatoid arthritis bone erosion. Methods: CIA rats induced by incomplete Freund’s adjuvant induced bovine collagen type Ⅱ, 60 Wistar rats were randomly divided into normal control group, model control group, methotrexate group, Hanbi Decoction , Middle and low dose groups. Methotrexate group was used as control to observe the effect of different doses of Hanbi Decoction on the expression of RANKL, RANK and OPG in bone of CIA rats. Results: Compared with the normal control group, the expression of RANKL m RNA, RANK m RNA, RANKL protein and RANK protein in osteoblasts increased and the expression of OPG m RNA and OPG protein decreased (P <0.01) in the model control group; Compared with the model control group, the expressions of RANKL m RNA, RANK m RNA, RANKL protein and RANK protein in each dose group and Methotrexate group of Hanbikang decoction decreased to some extent. The expression of OPG m RNA and OPG protein (P <0.01 or P <0.05), among which, Hanbifang Decoction was the most obvious in the high dose group and Hanbifang Decoction high dose group was not significantly different from the Methotrexate group (P <0.01 or P <0.05) > 0.05). Conclusion: Hanbi Decoction can inhibit the severity of arthritis in rats with CIA, increase the expression of OPG protein and gene in bone tissue and inhibit the protein and gene expression of RANKL and RANK, suggesting its anti-rheumatoid arthritis effect on bone erosion , The mechanism may be related to regulating OPG / RANKL / RANK osteoclast differentiation regulation signal transduction system.