摘要
目的研究甲基异茜草素抑制骨吸收的细胞学机制。方法采用原代培养的成骨细胞和骨髓单核细胞联合培养的方法,在1,25-(OH)2VitaminD3和地塞米松作用下,使骨髓单核细胞分化形成破骨细胞。磷酸苯二钠法测定破骨细胞抗酒石酸酸性磷酸酶(Tartrate-resistant acid phosphatase,TRAP)的活性;计算机图像分析技术测定骨片上破骨细胞性骨吸收陷窝的面积;荧光酶标方法测定组织蛋白酶K的活性。结果甲基异茜草素在0.1~10μmo.lL-1范围内,浓度依赖性地抑制破骨细胞形成、分化、TRAP酶活性和在骨片上形成的吸收陷窝的数目和面积。结论甲基异茜草素通过抑制破骨细胞的形成、分化和骨吸收功能来减少骨质的丢失。
Aim To investigate the cellular mechanism of rubiadin inhibitory effects on bone resorption.Methods Multinucleated osteoclasts were induced by 1,25-dihydroxyvitamine D 3 and dexamethasone from bone marrow cells and cocultured with primary osteoblastic cells.The activity of TRAP was measured by p-nitrophenyl sodium phosphate assay.The bone resorption pit area on the bone slices formed by osteoclast was measured by computer image processing.The cathepsin K was measured by fluorescence microplate reader.Results At the concentration of 0.1,1 and 10μmol · L^-1,rubiadin dose-dependently suppressed the formation of TRAP-positive multinucleated cells,the TRAP activity and the osteoclastic bone resorption.Conclusion Rubiadin can decrease bone loss through the inhibition of osteoclast formation,differentiation and bone resorption.
出处
《解放军药学学报》
CAS
2009年第6期505-509,共5页
Pharmaceutical Journal of Chinese People's Liberation Army