Objective:To investigate the formation of stress granule (SG) in human periodontal ligament cells (hPDLCs) under stress, and its effect on the apoptosis, the expression of inflammatory factors, and the generation of reactive oxygen species (ROS) under lipopolysaccharide (LPS) stimulation.Methods:Sodium arsenite (SA) was used to induce SG formation in hPDLCs, and immunofluorescence staining was used to quantify SG formation. Live and dead cell staining, real-time quantitative polymerase chain reaction (RT-qPCR) and immunofluorescence staining were used to detect the localization and expression of cysteinyl aspartate-specific proteinase 3 (Caspase-3) in hPDLCs to evaluate the effect of SG formation on apoptosis. RT-qPCR was used to detect the mRNA expression changes of inflammatory-related cytokines interleukin 1β (IL-1β) and interleukin 6 (IL-6) during LPS stimulation. ROS detection was used to assess the effect of SG on LPS-induced ROS levels of hPDLCs.Results:SA successfully induced SG formation in hPDLCs. The results of immunofluorescence staining showed that Caspase-3 was localized in SG, which significantly inhibited the apoptosis of hPDLCs. RT-qPCR results indicated that SG could downregulate the mRNA relative expression of LPS-stimulated inflammatory cytokines in hPDLCs. ROS detection showed that SG inhibited LPS-induced ROS generation in hPDLCs.Conclusion:SG can protect hPDLCs from stress-induced apoptosis and inhibit the expression of LPS-triggered inflammatory-related factors and ROS generation.