Hispolon Suppresses Endoplasmic Reticulum Stress and Apoptosis of Periodontal Ligament Cells in Periodontitis

Abstract

In periodontitis, increased endoplasmic reticulum stress followed by apoptosis and cell death in periodontal ligament cells further exacerbates periodontium destruction. Hispolon, a traditional Chinese medicine, could attenuate cell death induced by excessive oxidation. However, its role in oxidative stress and apoptosis in periodontitis is still unclear. To this end, the effect of the increasing dosage of hispolon on the reversal of the increase in cell viability caused by lipopolysaccharide in periodontal ligament cells in a periodontitis cell model was evaluated. The results show a dose-dependent hispolon promotion of cell viability in periodontal ligament cells. Cells treated with hispolon exhibited a decrease in cell apoptosis and a reduction in endoplasmic reticulum stress (Activating Transcription Factor 4, Glucose-Regulated Protein 78, and C/EBP-homologous protein) and inflammation (tumor necrosis factor-α, Interleukin-18, and Interleukin-6) levels than the lipopolysaccharide alone group. To further investigate the underlying mechanism(s), the relative expression of phosphorylation of extracellularly regulated protein kinases and phosphorylation of Jun N-terminal kinase in periodontal ligament cells were measured. The results show that hispolon attenuated lipopolysaccharide-induced inhibition of endoplasmic reticulum stress and apoptosis by deactivating the mitogen-activated protein kinase signaling pathway. In conclusion, hispolon reduces endoplasmic reticulum stress and alleviates apoptosis of periodontal ligament cells in periodontitis, and the protective mechanism is associated with the deactivation of the mitogen-activated protein kinase signaling pathway.