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首页> 外文期刊>Oral diseases >Mineral trioxide aggregate enhances the odonto/osteogenic capacity of stem cells from inflammatory dental pulps via NF-rB pathway
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Mineral trioxide aggregate enhances the odonto/osteogenic capacity of stem cells from inflammatory dental pulps via NF-rB pathway

机译：三氧化二矿物聚集体通过NF-rB途径增强发炎牙髓干细胞的牙本质/成骨能力

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OBJECTIVE: This study was designed to investigate the effects of mineral trioxide aggregate (MTA) on the osteo/odontogenic differentiation of inflammatory dental pulp stem cells (iDPSCs).MATERIALS AND METHODS: inflammatory DPSCs were isolated from the inflammatory pulps of rat incisors and cocultured with MTA-conditioned medium. MTT assay and flow cytometry were performed to evaluate the proliferation of iDPSCs. Alkaline phosphatase (ALP) activity, alizarin red staining, real-time RT-PCR, and Western blot assay were used to investigate the differentiation capacity as well as the involvement of NF-kB pathway in iDPSCs.RESULTS: Mineral trioxide aggregate-treated iDPSCs demonstrated the higher ALP activity and formed more mineralized nodules than the untreated group. The odon-to/osteoblastic markers (Alp, Runx2/RUNX2, Osx/OSX, Ocn/OCN, and DspplDSP, respectively) in MTA-treated iDPSCs were significantly upregulated as compared with untreated iDPSCs. Mechanistically, cytoplastic phos-P65 and nuclear P65 in MTA-treated iDPSCs were significantly increased in a time-dependent manner. Moreover, the inhibition of NF-kB pathway suppressed the MTA-induced odonto/osteoblastic differentiation of iDPSCs, as indicated by decreased ALP levels, weakened mineralization capacity and downregulated levels of odonto/osteoblastic genes (Osx, Ocn, and Dspp).CONCLUSIONS: Mineral trioxide aggregate enhances the odonto/osteogenic capacity of DPSCs from inflammatory sites via activating the NF-kB pathway.
机译：目的：本研究旨在探讨三氧化二矿聚集体（MTA）对炎性牙髓干细胞（iDPSCs）骨/牙源性分化的影响。材料与方法：从大鼠切牙的炎性牙髓中分离炎性DPSCs并进行共培养用MTA条件培养基。进行MTT测定和流式细胞术以评估iDPSC的增殖。通过碱性磷酸酶（ALP）活性，茜素红染色，实时RT-PCR和Western印迹分析来研究iDPSCs的分化能力以及NF-kB途径的参与。与未处理组相比，ALP活性更高，形成了更多的矿化结节。与未经处理的iDPSC相比，经MTA处理的iDPSC中的Oto-to /成骨细胞标记（分别为Alp，Runx2 / RUNX2，Osx / OSX，Ocn / OCN和DspplDSP）显着上调。从机理上讲，MTA处理的iDPSC中的细胞增生性phos-P65和核P65以时间依赖性方式显着增加。此外，NF-kB途径的抑制抑制了MTA诱导的iDPSC的牙本质/成骨细胞分化，表现为ALP水平降低，矿化能力减弱以及牙本质/成骨细胞基因（Osx，Ocn和Dspp）的水平下调。三氧化二矿聚集体通过激活NF-kB途径增强了来自炎症部位的DPSC的牙本质/成骨能力。

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