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Purposes: Increased advanced glycation end products (AGEs) plays critical role in the exacerbation of periodontitis in diabetic patients. Though our previous findings confirmed the importance of endoplasmic reticulum stress (ERS) in diabetic-relative periodontitis, the regulating action of ERS on AGEs-induced apoptosis remains uncertain. Methods: human periodontal ligament cells (hPDLCs) were pretreated with ERS inducer tunicamycin or thapsigargin, followed by AGEs. Cell viability and expression ofGRP78 were analyzed. Results: AGEs decreased cell viability. Tunicamycin or thapsigargin pretreatment inhibited AGEs-induced cytotoxicity and increased the expression of GRP78. Knockdown of GRP78 significantly blunts the protective effect of tunicamycin or thapsigargin. Conclusion: These data suggest that tunicamycin or thapsigargin suppresses AGEs-induced cytotoxicity by upregulation of GRP78.

Endoplasmic Reticulum Stress Pretreatment Alleviated Advanced Glycation End Products-induced Cytotoxicity