Effect of oral malodorous compound on the osteoclast differentiation and alveolar bone loss.

口腔恶臭化合物对破骨细胞分化和牙槽骨丢失的影响。

• 批准号: 21592667
• 负责人: IMAI Toshio
• 金额: $ 2.91万
• 依托单位: The Nippon Dental University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2009
• 资助国家: 日本
• 起止时间: 2009 至 2011
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-21592667/
• 关键词: 予防歯科学; 口臭物質; 硫化水素; 破骨細胞; シグナル伝達; PKC; c-Raf; 骨髄由来細胞; 情報伝達機構; SMAD2/3; 口臭; 分化; RANKL

The objective of this study was to elucidate the signal transduction mechanisms of hydrogen sulfide-induced osteoclast differentiation in primary cultued osteoclast precursor cells and RAW264 cells. Hydrogen sulfide at physiologic concentrations in mouth air induced the differentiation of mouse bone marrow-derived osteoclast precursor cells in the absence of RANKL. Moreover, hydrogen sulfide activated ERK1/2 phosphorylation in the osteoclast precursor cells. A low concentrations of NaHS induced PKC phosphorylation in RAW 264 cells. When pretreatment with PKC inhibitor(GF109203x), NaHS-induced the activation of PKC, c-Raf and ERK1/2 in RAW264 cells were diminished. These results suggested that hydrogen sulfide at physiologic concentrations stimulate the osteoclast differentiation through the PKC, cRaf, ERK1/2 pathway.

这项研究的目的是阐明硫化氢诱导的破骨细胞分化的信号转导机制在原代培养的破骨细胞前体细胞和RAW264细胞中。硫化氢在口腔空气中的生理浓度诱导小鼠骨髓衍生的破骨细胞前体细胞的分化，在没有RANKL的情况下。此外，硫化氢激活了破骨细胞前体细胞中的ERK1/2磷酸化。低浓度的NAHS在RAW 264细胞中诱导PKC磷酸化。当用PKC抑制剂（GF109203X）预处理时，NAHS诱导了RAW264细胞中PKC，C-RAF和ERK1/2的激活。这些结果表明，生理浓度的硫化氢通过PKC，CRAF，ERK1/2途径刺激破骨细胞分化。