Icariin induces the growth, migration and osteoblastic differentiation of human periodontal ligament fibroblasts by inhibiting Toll-like receptor 4 and NF-κB p65 phosphorylation.

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)-4/nuclear 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.