Department of Conservative Dentistry, School of Dentistry, Wonkwang University, Iksan, Jeonbuk, Republic of Korea.
J Endod. 2010 Mar;36(3):447-52. doi: 10.1016/j.joen.2009.11.021. Epub 2010 Jan 25.
Although simvastatin has multiple demonstrable effects, its function in dentinogenesis remains unclear. In this study, we tested the hypothesis that the addition of simvastatin to human dental pulp cells (HDPCs) stimulates odontogenesis both by promoting odontoblastic differentiation and by favoring the release of angiogenic factors. In addition, the role of heme oxygenase-1 (HO-1) in these effects was investigated.
The expression of markers for odontoblastic differentiation and angiogenesis was analyzed by means of alkaline phosphatase (ALP) activity, alizarin red staining, and Western blotting.
Simvastatin enhanced the differentiation of HDPCs by up-regulating mineralization nodules and odontogenic markers as well as angiogenic markers. These phenomena were then correlated with the induction of HO-1 protein levels. The inducing effect of simvastatin on odontoblastic differentiation and angiogenesis was nullified by an HO-1 inhibitor and a carbon monoxide (CO) scavenger.
These results suggested that simvastatin exerts its odontoblastic differentiation and angiogenesis-inducing effects in HDPCs through a mechanism that involves the action of HO-1 and its product CO.
尽管辛伐他汀具有多种可证明的作用，但它在牙本质形成中的功能仍不清楚。在这项研究中，我们检验了这样一个假设，即辛伐他汀添加到人牙髓细胞（HDPCs）中，通过促进成牙本质细胞分化和有利于血管生成因子的释放来刺激牙发生。此外，还研究了血红素加氧酶-1（HO-1）在这些作用中的作用。
通过碱性磷酸酶（ALP）活性、茜素红染色和 Western blot 分析来分析成牙本质分化和血管生成的标志物表达。
辛伐他汀通过上调矿化结节和牙源性标志物以及血管生成标志物来增强 HDPCs 的分化。这些现象与 HO-1 蛋白水平的诱导相关。HO-1 抑制剂和一氧化碳（CO）清除剂可消除辛伐他汀对成牙本质细胞分化和血管生成的诱导作用。
这些结果表明，辛伐他汀通过涉及 HO-1 及其产物 CO 的作用，在 HDPCs 中发挥其成牙本质细胞分化和血管生成诱导作用。
