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P物质通过人牙髓细胞中COX-2的表达刺激RANKL的释放。

Substance P stimulates release of RANKL via COX-2 expression in human dental pulp cells.

作者信息

Kojima T, Yamaguchi M, Kasai K

机构信息

Department of Orthodontics, Nihon University School of Dentistry at Matsudo, 2-870-1 Sakaecho-Nishi, Matsudo City, Chiba, 271-8587, Japan.

出版信息

Inflamm Res. 2006 Feb;55(2):78-84. doi: 10.1007/s00011-005-0013-5.

DOI:10.1007/s00011-005-0013-5
PMID:16612568
Abstract

OBJECTIVE

Our previous study found that substance P (SP), a sensory neuropeptide, was expressed in the dental pulp of rats during experimental tooth movement. We examined the effects of SP on the production of prostaglandin (PG) E2 and the receptor activator of nuclear factor- B ligand (RANKL) by human dental pulp fi broblast-like (HDPF) cells.

MATERIALS AND METHODS

SP was added to cultured HDPF cells at concentrations ranging from of 10(-4) to 10(-12) mol/L. PGE2 and soluble RANKL (sRANKL) levels were determined using enzyme-linked immunosorbent assay kits. Gene expression was confi rmed by RT-PCR analysis. Pit formation assays using dentin slices were carried out to examine the effect of SP on osteoclastogenesis.

RESULTS

The levels of PGE2 and sRANKL increased in the presence of SP, though the increases were greater in the experimental groups in both a time- and concentration-dependent manner, and the increase of RANKL was partially mediated by PGE2. The gene expression of cyclooxygenase (COX)-2 and RANKL was up-regulated, and conditioned medium samples obtained from HDPF cells treated with SP induced bone resorption.

CONCLUSIONS

SP stimulated the production of PGE2 and RANKL, and promoted bone resorption. Therefore, SP may be involved in pulpal inflammation and root resorption during orthodontic tooth movement.

摘要

目的

我们之前的研究发现,感觉神经肽P物质(SP)在实验性牙齿移动过程中在大鼠牙髓中表达。我们研究了SP对人牙髓成纤维样(HDPF)细胞前列腺素(PG)E2产生及核因子-κB受体激活剂配体(RANKL)的影响。

材料与方法

将浓度范围为10^(-4)至10^(-12)mol/L的SP添加到培养的HDPF细胞中。使用酶联免疫吸附测定试剂盒测定PGE2和可溶性RANKL(sRANKL)水平。通过逆转录-聚合酶链反应(RT-PCR)分析确认基因表达。使用牙本质切片进行凹坑形成试验,以研究SP对破骨细胞生成的影响。

结果

在SP存在下,PGE2和sRANKL水平升高,尽管在实验组中升高幅度更大,呈时间和浓度依赖性,且RANKL的增加部分由PGE2介导。环氧合酶(COX)-2和RANKL的基因表达上调,用SP处理的HDPF细胞获得的条件培养基样本诱导骨吸收。

结论

SP刺激PGE2和RANKL的产生,并促进骨吸收。因此,SP可能参与正畸牙齿移动过程中的牙髓炎症和牙根吸收。

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