Proanthocyanidins (PA) have been proven to suppress inflammation and promote osteogenic differentiation. However, whether PA could promote osteogenic differentiation of human periodontal ligament fibroblasts (HPDLFs) in inflammatory environment is unclear. Here, HPDLFs were stimulated by tumor necrosis factor-α (TNF-α), PA, or their combination, and osteogenic differentiation- and mineralization-associated markers were detected by quantitative real-time polymerase chain reaction (qRT-PCR), alizarin red S staining, and alkaline phosphatase (ALP) activity assay. The result showed that PA significantly upregulated expression of osteogenesis-related genes and proteins and ALP activity in HPDLFs compared with the control in non-inflammatory environment. Moreover, PA significantly reversed inhibition of osteogenesis-related gene and protein expression, ALP activity, and mineralization caused by TNF-α. The underlying mechanism was that PA could regulate osteogenesis of HPDLFs via suppressing nuclear factor-kappa beta (NF-κB) signal pathway. These findings suggest that PA may contribute to bone generation in inflammatory microenvironment via suppressing NF-κB signal pathway. Thus, PA may be a potential treatment agent for periodontal bone regeneration.
Keywords: human periodontal ligament fibroblasts (HPDLFs); nuclear factor-kappa beta (NF-κB) signal pathway; osteogenic differentiation; proanthocyanidins; tumor necrosis factor-α (TNF-α).