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机构地区:[1]中南大学湘雅二医院代谢内分泌研究所,长沙410011
出 处:《中国骨质疏松杂志》2006年第4期342-345,共4页Chinese Journal of Osteoporosis
摘 要:目的探讨甲状旁腺激素(PTH)调节骨吸收作用的途径和机理。方法用0.2~20μgPTH干预人成骨肉瘤MG63细胞2d,观察PTH对MG63细胞表达护骨素(OPG)、护骨素配体(OPGL)及其相关因子,如肿瘤坏死因子相关性凋亡诱导配体(TRAIL)、巨噬细胞集落刺激因子(MCSF)的影响,用RTPCR法检测OPG、OPGL、MCSF和TRAILmRNA表达情况,用Westernblot分析法检测OPG和OPGL蛋白表达情况。结果PTH下调MG63细胞中OPG的表达,上调OPGL、MCSF及TRAIL的表达。结论PTH能够减低成骨样细胞MG63中OPGOPGL表达比率,增加MCSF、TRAIL的表达。这可能有利于促进破骨细胞生成及活化,进而促进骨吸收。Objective To investigate the pathway and mechanism of parathyroid hormone (PTH) in regulating bone resorption. Methods MG 63 cells were treated with different dosages of PTH (0.2 ~ 20 μg) for 2 days and the regulatory effects of parathyroid hormone (PTH) was observed on the expressions of osteoprotegerin(OPG), the ligand of osteoprotegerin (OPGL) and the related cytokines (M-CSF and TRAIL) in MG 63 cells. The expressions of OPG, OPGL, M-CSF and TRAIL mRNA were detected by RT-PCR. The expressions of OPG and OPEL protein were measured by Western blot. Results The expression of OPG was down-regulated by PTH, but the expression of OPEL, M-CSF and TRAIL was up-regulated in MG 63 cells. Conclusions PTH could decrease the expression of OPG, but increase the expressions of OPGL, M-CSF and TRAIL in osteoblast-like cells, which is helpful to stimulate osteoclast differentiation and activity and further potentiate bone resorption and bone loss.
关 键 词:PTH MG 63细胞 护骨素/护骨素配体(OPG/OPGL)
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