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地塞米松、抗坏血酸和β-甘油磷酸通过调节雌激素受体和骨桥蛋白表达对成骨细胞分化的影响。

The effects of dexamethasone, ascorbic acid, and β-glycerophosphate on osteoblastic differentiation by regulating estrogen receptor and osteopontin expression.

机构信息

Department of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science and Technology, Seoul National University, Seoul, Korea.

出版信息

J Surg Res. 2012 Mar;173(1):99-104. doi: 10.1016/j.jss.2010.09.010. Epub 2010 Oct 8.

DOI:10.1016/j.jss.2010.09.010
PMID:21035140
Abstract

BACKGROUND

Ascorbic acid (AA), β-glycerophosphate (GP), and dexamethasone (DEX) are the compounds known to favor the expression of the osteoblastic phenotype in several bone cell systems.

MATERIALS AND METHODS

In this report, the combination effects of differentiation agents on osteoprecursor cells were evaluated. The effect on cell proliferation was determined by a cell viability test with morphologic analysis. Differentiation and mineralization were evaluated using an alkaline phosphatase activity test and alizarin red-S staining. Protein expressions related to bone formation, such as transforming growth factor-beta (TGF-β), estrogen receptor-alpha (ER-α), and osteopontin (OPN) were evaluated by using a Western blot analysis.

RESULTS AND CONCLUSION

AA and GP provided an inductive effect for differentiation of osteoprecusor cells, while short-term application of DEX seemed to lead to a dose-dependent increase of cellular differentiation. Long-term use of DEX seemed to reduce mineralization. These effects may seem to be regulated by the expression of ER-α, OPN, and TGF-β. Further studies related to this mechanism within the in vivo model may be necessary to ascertain greater detail.

摘要

背景

抗坏血酸(AA)、β-甘油磷酸(GP)和地塞米松(DEX)是几种骨细胞系统中促进成骨表型表达的已知化合物。

材料和方法

在本报告中,评估了分化剂对成骨前体细胞的组合效应。通过细胞活力试验和形态分析来确定对细胞增殖的影响。通过碱性磷酸酶活性试验和茜素红 S 染色评估分化和矿化。通过 Western blot 分析评估与骨形成相关的蛋白表达,如转化生长因子-β(TGF-β)、雌激素受体-α(ER-α)和骨桥蛋白(OPN)。

结果和结论

AA 和 GP 为成骨前体细胞的分化提供了诱导作用,而 DEX 的短期应用似乎导致细胞分化的剂量依赖性增加。DEX 的长期使用似乎会减少矿化。这些作用可能受 ER-α、OPN 和 TGF-β 的表达调控。为了更详细地确定这一机制,可能需要在体内模型中进行相关的进一步研究。

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