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以VitD3为诱发药物,成功建立起大鼠动脉钙化模型,用免疫组化法检测了骨保护素(osteoprotegrin,OPG)、核因子kB受体激活物配体(receptor activator of nuclear factor kappaB ligand,RANKL)在血管组织中的表达,同时测定了血管组织中钙含量及碱性磷酸酶活性.结果显示,与正常对照组相比,VitD3处理组血管组织OPG表达明显减少而RANKL表达明显增加,血管组织钙含量及碱性磷酸酶活性明显增高;与VitD3处理组比较,鲑鱼降钙素治疗组血管钙化程度明显减轻,血管组织OPG表达明显增加而RANKL表达明显减少,血管组织钙含量及碱性磷酸酶活性明显降低.本研究结果表明OPG/RANKL参与血管钙化的调节,鲑鱼降钙素可能通过OPG/RANKL途径有效抑制血管钙化.
VitD3-induced drug was used to establish rat model of arterial calcification. Immunohistochemistry was used to detect the expression of osteoprotegrin (OPG), receptor activator of nuclear factor kappaB ligand (RANKL ) In blood vessel and the content of calcium and the activity of alkaline phosphatase in vascular tissue were measured at the same time.The results showed that compared with the normal control group, the expression of OPG in the vascular tissue of VitD3 group was significantly decreased and the expression of RANKL was significantly increased Calcium content and alkaline phosphatase activity were significantly increased; Compared with VitD3 treatment group, salmon calcitonin treatment group significantly reduced the degree of vascular calcification, vascular tissue OPG expression was significantly increased RANKL expression was significantly reduced, vascular tissue calcium content and alkaline phosphatase Activity significantly reduced.The results of this study show that OPG / RANKL involved in the regulation of vascular calcification, salmon calcitonin via OPG / RANKL pathway may be effective in inhibiting vascular calcification.