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P物质通过激活破骨细胞前体中的核因子κB来上调破骨细胞生成。

Substance P upregulates osteoclastogenesis by activating nuclear factor kappa B in osteoclast precursors.

作者信息

Sohn Soo Joon

机构信息

Department of Otolaryngology, Catholic University of Daegu School of Medicine, Daegu, South Korea.

出版信息

Acta Otolaryngol. 2005 Feb;125(2):130-3. doi: 10.1080/00016480410017710.

Abstract

CONCLUSION

SP upregulates osteoclastogenesis by activating NF-kappaB in osteoclast precursors.

OBJECTIVE

Osteoclastic bone resorption is a common finding of otitis media with or without cholesteatoma. Factors upregulating osteoclastogenesis are implicated in bone resorption. The aim of this study was to investigate the effect of substance P (SP) on mouse osteoclastogenesis in vitro.

MATERIAL AND METHODS

The SP dose response was analyzed in a mouse osteoclast culture induced by macrophage colony-stimulating factor and receptor activator for nuclear factor kappa B (NF-kappaB) ligand. Western blot analysis was performed to elucidate the subcellular target of SP in osteoclastogenesis.

RESULTS

Treatment with SP significantly increased osteoclastogenesis compared to control. SP activated nuclear translocation of NF-kappaB, which is an essential event in osteoclastogenesis in osteoclast precursors (bone marrow macrophages).

摘要

结论

P物质通过激活破骨细胞前体中的核因子κB上调破骨细胞生成。

目的

破骨细胞性骨吸收是伴或不伴胆脂瘤中耳炎的常见表现。上调破骨细胞生成的因素与骨吸收有关。本研究旨在探讨P物质(SP)对体外小鼠破骨细胞生成的影响。

材料与方法

在由巨噬细胞集落刺激因子和核因子κB受体激活剂(NF-κB配体)诱导的小鼠破骨细胞培养中分析SP剂量反应。进行蛋白质印迹分析以阐明SP在破骨细胞生成中的亚细胞靶点。

结果

与对照组相比,SP处理显著增加破骨细胞生成。SP激活核因子κB的核转位,这是破骨细胞前体(骨髓巨噬细胞)破骨细胞生成中的一个关键事件。

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