LAUSR

This study was aimed to investigate the role of Sirt1 in LPS-injured periodontal ligament fibroblast (PDLF), to evaluate potential functions of Sirt1 in the pathogenesis of periodontitis. Sirt1 overexpression significantly increased cell viability, Ki67 positive cell number and PCNA expression in LPS-injured PDLF, and vice versa. Cell apoptosis was significantly decreased, and the release of pro-inflammatory cytokines (IL-1α, IL-6, IL-8 and TNF-α) was significantly reduced when Sirt1 was overexpressed. Sirt1 overexpression down-regulated toll-like receptor 4 (TLR4), and inhibited the JNK/NF-κB pathways; while knockdown of Sirt1 up-regulated TLR4, and activated JNK/NF-κB pathways. To conclude, Sirt1 alleviates inflammation of PDLF induced by LPS through down-regulation of TLR4 and inactivation of JNK/NF-κB pathways.