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首页> 外文期刊>Molecular medicine reports >Icariin induces the growth, migration and osteoblastic differentiation of human periodontal ligament fibroblasts by inhibiting Toll-like receptor 4 and NF-kappa B p65 phosphorylation
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Icariin induces the growth, migration and osteoblastic differentiation of human periodontal ligament fibroblasts by inhibiting Toll-like receptor 4 and NF-kappa B p65 phosphorylation

机译:icariin通过抑制Toll样受体4和NF-Kappa B P65磷酸化来诱导人牙周韧带成纤维细胞的生长,迁移和骨质细胞分化

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The proliferation, migration and differentiation capacities of human periodontal ligament fibroblasts (HPDLCs) are important for the treatment of periodontal diseases. The aim of the present study was to investigate whether icariin could promote these abilities in HPDLCs, and explore the cellular mechanisms therein. The results indicated that icarrin markedly blocked apoptosis, and increased the viability and migration of HPDLCs, particularly at the concentrations of 20 and 50 mu M. In addition, icariin significantly promoted HPDLCs to synthesize extracellular matrix, which was reflected by the decreased expression of matrix matalloproteinase-1 and increased expression of tissue inhibitor of metalloproteinase-1. Furthermore, the levels of bone morphogenetic protein 2, collagen I, osteoprotegerin and alkaline phosphatase were markedly elevated by icariin, indicating that icariin was able to promote the osteogenic differentiation capability of HPDLCs. Icariin also inactivated the Toll-like receptor 4 (TLR)-4/nuclear factor (NF)-kappa B signaling pathway by suppressing the expression levels of TLR-4 and phosphorylated p65, and by blocking p65 nuclear translocation. These results suggested that icarrin increased the survival, migration and osteoblastic differentiation of HPDLCs by inhibiting the TLR-4/NF-kappa B signaling pathway.
机译:人牙周韧带成纤维细胞(HPDLC)的增殖,迁移和分化能力对于治疗牙周病是重要的。本研究的目的是探讨淫羊藿苷是否可以促进HPDLC中的这些能力,并探索其中的细胞机制。结果表明,Icarrin显着阻断了细胞凋亡,并增加了HPDLC的活力和迁移,特别是在20和50μm的浓度下。此外,Icariin显着促进了HPDLC,以合成细胞外基质,这反映了基质的表达式反映金属蛋白酶-1和组织抑制剂的增加表达式抑制剂-1。此外,通过乙素蛋白显着升高了骨形态发生蛋白2,胶原蛋白I,骨蛋白酶和碱性磷酸酶的水平,表明伊加里宁能够促进HPDLC的成骨分化能力。 icariin还通过抑制TLR-4和磷酸化P65的表达水平,并通过阻断P65核易位来灭活Toll样受体4(TLR)-4 /核因子(NF)-Kappa发信号通路。这些结果表明,Icarrin通过抑制TLR-4 / NF-κB信号通路来增加HPDLC的存活率,迁移和骨质细胞分化。

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