Fluocinolone Acetonide Promotes the Proliferation and Mineralization of Dental Pulp Cells
Fluocinolone Acetonide Promotes the Proliferation and Mineralization of Dental Pulp Cells
复制标题
氟轻松促进牙髓细胞增殖和矿化
DOI：
10.1016/j.joen.2012.09.012
复制
发表时间：
2013-02-01
影响因子：
4.2
通讯作者：
Wang, Xinzhi
中科院分区：
文献类型：
--
作者：
Liu, Zhongning;Jiang, Ting;Wang, Xinzhi
简介：本研究旨在探讨氟轻松对人牙髓细胞增殖和矿化的影响。评价氟轻松对修复性牙本质形成和损伤牙髓修复的潜在作用。方法：采用八肽胆囊收缩素法和流式细胞术检测醋酸氟轻松对DPC增殖的影响。通过碱性磷酸酶（ALP）组织化学染色、ALP活性、免疫组化、茜素红染色和逆转录聚合酶链反应检测矿化相关生物标志物（包括ALP、骨唾液蛋白和骨钙素），研究氟轻松的矿化作用。采用实时荧光定量聚合酶链反应（PCR）和免疫印迹（Westernblot）技术检测牙本质涎磷蛋白和Wnt 4等参与矿化过程的分子。结果：低浓度醋酸氟轻松（0.1 ~ 40 μ mol/L）促进DPC增殖;流式细胞术结果显示，1和10 μ mol/L的醋酸氟轻松分别作用48小时后，DPC的CD 146阳性亚群显著增加。氟轻松组早期矿化标志物ALP、中期矿化标志物骨唾液蛋白和晚期矿化标志物骨钙素mRNA表达和活性均明显高于对照组。氟轻松组Wnt 4和牙本质特异性标志物牙本质涎磷蛋白表达较对照组明显上调。结论：醋酸氟轻松可促进DPC增殖，尤其是对CD 146+细胞亚群的增殖。醋酸氟轻松可促进牙本质前体细胞的矿化，对损伤牙髓组织具有潜在的修复作用。（J Endod 2013;39：217-222）
Introduction: The aim of this study was to investigate the role of the steroid fluocinolone acetonide on the proliferation and mineralization of human dental pulp cells (DPCs). The potential effect of fluocinolone acetonide on reparative dentin formation and the recovery of injured dental pulp were evaluated. Methods: The proliferative effect of fluocinolone acetonide on DPCs was analyzed by cholecystokinin octapeptide assay and flow cytometry. The mineralized effect of fluocinolone acetonide was investigated by the detection of mineralization-related biomarkers including alkaline phosphatase (ALP), bone sialoprotein, and osteocalcin by using ALP histochemical staining, ALP activity, immunostaining, alizarin red staining, and reverse-transcriptase polymerase chain reaction. The molecules, including dentin sialophosphoprotein and Wnt4, involved in the process of mineralization were detected by real-time polymerase chain reaction and Western blot analysis. Results: Low concentrations of fluocinolone acetonide (0.1-40 mu mol/L) promoted the proliferation of DPCs. The flow cytometry results showed that the CD146-positive subpopulation of DPCs was significantly increased after treatment with fluocinolone acetonide at 1 and 10 mu mol/L for 48 hours, respectively. The messenger RNA expression and activity of the early-stage mineralization marker ALP were evidently increased in fluocinolone acetonide treated DPCs compared with the untreated control group, so did the middle-stage mineralization marker bone sialoprotein and the late-stage mineralization marker osteocalcin. Meanwhile, Wnt4 and the dentin-specific marker dentin sialophosphoprotein were obviously up-regulated by fluocinolone acetonide compared with the untreated controls. Conclusions: Fluocinolone acetonide can promote the proliferation of DPCs, especially for the CD146+ subpopulation. Fluocinolone acetonide can initiate the mineralization of DPCs and has the potential role in repairing injured pulp tissues. (J Endod 2013;39:217-222)