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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-κB p65 phosphorylation

机译:Icariin通过抑制Toll样受体4和NF-κBp65磷酸化诱导人牙周膜成纤维细胞的生长迁移和成骨细胞分化

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摘要

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 µM. 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)-4uclear factor (NF)-κB 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-κB signaling pathway.
机译:人牙周膜成纤维细胞(HPDLC)的增殖,迁移和分化能力对于牙周疾病的治疗很重要。本研究的目的是研究甘菊酯是否可以在HPDLCs中增强这些能力,并探索其中的细胞机制。结果表明,伊卡林显着阻断细胞凋亡,并增加了HPDLC的活力和迁移,特别是在20和50 µM的浓度下。此外,icariin显着促进HPDLCs合成细胞外基质,这通过基质金属蛋白酶1的表达减少和组织金属蛋白酶1的表达增加来反映。此外,二十碳三烯显着提高了骨形态发生蛋白2,胶原蛋白I,骨保护素和碱性磷酸酶的水平,表明二十碳三烯能够促进HPDLCs的成骨分化能力。通过抑制TLR-4和磷酸化的p65的表达水平,以及通过阻断p65的核易位,伊卡瑞林还可以使Toll样受体4(TLR)-4 /核因子(NF)-κB信号通路失活。这些结果表明,依卡琳通过抑制TLR-4 /NF-κB信号通路增加了HPDLC的存活,迁移和成骨细胞分化。

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