Tetramethylpyrazine reduces inflammation levels and the apoptosis of LPS-stimulated human periodontal ligament cells via the downregulation of miR-302b

Periodontitis is the main cause of tooth or tissue loss. Human periodontal ligament stem cells (hPDLSCs), which have high proliferative, self-renewal and multi-differentiation abilities, are vital for the restoration of periodontitis-induced injuries. The anti-inflammatory and anti-apoptotic agent, tetramethylpyrazine (TMP), is a promising agent used for the protection of PDLSCs from apoptosis and inflammation induced by periodontitis. The aim of the present study was to investigate the effects of TMP on lipopolysaccharide (LPS)-stimulated hPDLSCs. LPS-stimulated hPDLSCs were established as the cell model. CCK-8 assay was performed to evaluate cell viability, western blot analysis was performed to measure protein expression and flow cytometry was performed to detect cell apoptosis levels. Detection kits were used to evaluate the levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6. Reverse transcription-quantitative PCR analysis was performed to detect gene expression. TMP alleviated the effects of LPS on cell viability, inflammation levels and cell apoptosis. TMP downregulated microRNA (miR)-302b levels in LPS-stimulated cells. Transfection with miR-302b mimic reversed the anti-inflammatory and anti-apoptotic effects of TMP on LPS-stimulated cells. TMP reduced inflammation and the apoptosis of LPS-stimulated human periodontal ligament cells via the downregulation of miR-302b. The anti-inflammatory and anti-apoptotic effects exerted by TMP render it a promising agent for the protection of PDLSCs from injuries induced by periodontitis. The findings of the present study may aid in the development of a novel strategy for the treatment of periodontitis and may pave the way for further research.