骨松安促进骨质疏松大鼠骨折愈合的信号通路研究  

Study of Signal Pathway of Gusongan Promoting Fracture Healing in Rats with Osteoporosis

作　　者：江涛 侯秋科[2] 陈善创 刘子桃 刘启宇 苏海涛 黄永铨 JIANG Tao;HOU Qiuke;CHEN Shanchuang;LIU Zitao;LIU Qiyu;SU Haitao;HUANG Yongquan(The Second Affiliated Hospital of Guangzhou University of Chinese Medicine,Guangzhou 510006,China;The First Affiliated Hospital of Guangzhou University of Chinese Medicine,Guangzhou 510405,China)

机构地区：[1]广州中医药大学第二附属医院,广州510006 [2]广州中医药大学第一附属医院

出　　处：《中国中医骨伤科杂志》2021年第12期6-11,共6页Chinese Journal of Traditional Medical Traumatology & Orthopedics

基　　金：国家自然科学基金青年基金(82004387);广东省自然科学基金(2018A030313694)。

摘　　要：目的:初步探索影响骨松安促进骨质疏松大鼠骨折愈合的信号通路。方法:建立骨质疏松骨折大鼠模型,采用院内制剂骨松安胶囊进行治疗,7,14,21 d后采用ELISA法检测血清OPG、RANKL的表达,同时取出骨折端骨痂,采用Masson染色检测骨折端胶原蛋白变化,并采用免疫组化检测OPG、RANKL的表达。结果:在骨折后不同时期,骨松安治疗均可明显促进骨折端软骨细胞增殖,促进纤维胶原形成;ELISA、免疫组化结果显示OPG在治疗7 d及14 d表达持续上升,到21 d达到顶峰,与没有骨松安治疗大鼠相比,差异有统计学意义(P<0.05)。RANKL在骨折早期处于较高水平,骨质疏松骨折组大鼠最为明显,而骨松安治疗可明显抑制其表达,与没有骨松安治疗比较,差异有统计学意义(P<0.05)。骨松安治疗组OPG/RANKL比值较无骨松安治疗组高,治疗14 d最高,到21 d有所下降,差异均有统计学意义(P<0.05)。结论:骨松安可调控OPG/RANKL信号通路,抑制破骨细胞分化与成熟,抑制骨吸收,从而促进骨形成,能有效促进骨折愈合。Objective:To explore the signal pathways that affects Gusongan’s promotion of fracture healing in osteoporotic rats.Methods:A rat model of osteoporotic fracture was established and treated with Gusongan Capsules.After 7,14 and 21 d, the expression of serum OPG and RANKL was detected by ELISA.At the same time, the bone callus at the fractured end was taken out.Masson staining was used to detect the changes of collagen at the fracture end, and immunohistochemistry was used to detect the expression of OPG and RANKL.Results:In different periods after fracture, gusongan significantly promoted the proliferation of chondrocytes at the fracture end and promote the formation of fibrous collagen;ELISA and immunohistochemistry results showed that the expression of OPG increased continuously at 7 and 14 d of treatment, and reaches the peak at 21 st day.Compared with rats without Gusongan treatment, the difference was statistically significant.RANKL was at a high level in the early stage of fracture, which was most obvious in the osteoporotic fracture group, while the treatment with Gusongan significantly inhibited its expression.Compared with rats without Gusongan treatment, the difference was statistically significant.The OPG/RANKL ratio of the Gusongan treatment group was higher than that of the no gusongan treatment group, and reached the highest level in the 14 th day and decreased in the 21 st day.The differences were statistically significant.Conclusion:Gusongan can regulate OPG/RANKL signaling pathway, inhibit osteoclast differentiation and maturation and inhibit bone resorption, thereby promote bone formation and effectively promote fracture healing.

关 键 词：骨松安 破骨细胞 骨吸收 骨质疏松 骨折愈合 

分 类 号：R285.5[医药卫生—中药学]