Yanagita Manabu, Kashiwagi Yoichiro, Kobayashi Ryohei, Tomoeda Miki, Shimabukuro Yoshio, Murakami Shinya
Department of Periodontology, Division of Oral Biology and Disease Control, Osaka University Graduate School of Dentistry, Osaka, Japan.
J Endod. 2008 Sep;34(9):1061-5. doi: 10.1016/j.joen.2008.06.005.
Nicotine is a major component of tobacco smoke, and signals via nicotinic acetylcholine receptors (nAChR). However, little is known about the effects of nicotine on human dental pulp cells (HDPCs). In this study, we assessed the effects of nicotine on mineralization in HDPCs. We confirmed messenger RNA expression of nAChR subunits and examined the effects of nicotine on expression of extracellular matrices (ECMs), alkaline phosphatase (ALP) activity, and mineralized nodule formation by HDPCs. Gene expression of nAChR subunits alpha1, alpha2, alpha 4, alpha 5, alpha 6, alpha 7, beta1, beta2, and beta 4 was detected in HDPCs. Interestingly, the messenger RNA expression of dentin matrix acidic phosphoprotein-1, bone sialoprotein, and ALP activity were significantly reduced in nicotine-treated HDPC. In addition, mineralized nodule formation, which was examined by alizarin red staining, was also inhibited in HDPCs by the same treatment. These results indicate that nicotine suppresses the cytodifferentiation and mineralization of HDPCs, possibly via nAChR.
尼古丁是烟草烟雾的主要成分，通过烟碱型乙酰胆碱受体（nAChR）发挥信号作用。然而，关于尼古丁对人牙髓细胞（HDPCs）的影响却知之甚少。在本研究中，我们评估了尼古丁对HDPCs矿化的影响。我们证实了nAChR亚基的信使核糖核酸表达，并检测了尼古丁对细胞外基质（ECM）表达、碱性磷酸酶（ALP）活性以及HDPCs矿化结节形成的影响。在HDPCs中检测到了nAChR亚基α1、α2、α4、α5、α6、α7、β1、β2和β4的基因表达。有趣的是，在尼古丁处理的HDPCs中，牙本质基质酸性磷酸蛋白-1、骨涎蛋白的信使核糖核酸表达以及ALP活性均显著降低。此外，通过茜素红染色检测的矿化结节形成在相同处理的HDPCs中也受到抑制。这些结果表明，尼古丁可能通过nAChR抑制HDPCs的细胞分化和矿化。
