论文部分内容阅读
目的探讨淫羊藿素(IT)与核因子-κB受体活化因子配体(RANKL)蛋白靶点结合能力,并阐明其抗骨质疏松作用机制。方法采用分子对接技术模拟并预测RANKL与IT的相互作用,并通过切除大鼠双侧卵巢制备骨质疏松模型,评价IT对模型大鼠体质量、骨吸收血清指标碱性磷酸酶(ALP)和抗酒石酸盐酸性磷酸酶-5b(TRACP-5b)、骨密度(BMD)以及骨组织形态的调节作用。结果 IT可与靶蛋白RANKL发生稳定对接,IT组大鼠体质量较模型组显著降低(P<0.05),IT能显著降低模型大鼠血清ALP、TRACP-5b水平(P<0.01),显著降低模型大鼠股骨表面积与体积比值(BS/BV)、骨小梁分离度(Tb.Sp)值(P<0.01),显著增加BMD、骨体积分数(BV/TV)、骨小梁厚度(Tb.Th N)、骨小梁数目(Tb.N)值(P<0.01)。结论 IT能通过与RANKL蛋白靶点结合,抑制破骨细胞分化并发挥抗骨质疏松作用。
Objective To investigate the binding ability of icariin (IT) to the target of nuclear factor-kappa B receptor activator ligand (RANKL) and elucidate its anti-osteoporosis mechanism. Methods The molecular docking technique was used to simulate and predict the interaction between RANKL and IT. The model of osteoporosis was established by excision of both ovaries in rats. The effects of IT on the body weight, serum ALP and Tartrate-resistant acid phosphatase-5b (TRACP-5b), bone mineral density (BMD) and bone morphological regulation. Results IT could stably interface with target protein RANKL. The body weight of IT group was significantly lower than that of the model group (P <0.05), IT significantly reduced the level of serum ALP and TRACP-5b (P <0.01) (BS / BV) and trabecular separation (Tb.Sp) (P <0.01), significantly increased BMD, BV / TV, and trabecular thickness .Th N) and trabecular number (Tb.N) (P <0.01). Conclusion IT can inhibit osteoclast differentiation and exert anti-osteoporosis by binding with RANKL protein target.