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DOI

10.1016/j.jds.2024.11.033

First Page

1060

Last Page

1067

Abstract

Abstract Background/Purpose Triethylene-glycol-dimethacrylate (TEGDMA) is one of the monomers used in composite resin matrix. Residual TEGDMA can be eluted from bulk fill composite resins and the amounts also increased with time. Composite resin used as root-end filling materials may invoke the critical biologic reactions in surrounding tissues. However, little is known about the effects of TEGDMA on cementoblasts. The aim of this study was to investigate the possible detrimental effects of murine cementoblast (OCCM.30) by TEGDMA in vitro. Materials and methods OCCM.30 cells were exposed to TEGDMA (0, 1, 2, 4 mM) for 24 h. Cell viability was determined by microculture tetrazolium assay. Flow cytometry was conducted to evaluate the cell cycle distribution and the type of cell death. Caspase-mediated apoptotic cascade and mitogen-activated protein kinase (MAPK) pathways were analyzed by Western blot. Results The concentrations of TEGDMA≧1 mM were found to significantly inhibit OCCM.30 cell viability in a dose-dependent manner ( P < 0.05). TEGDMA dose-dependently induced apoptosis by the increase of sub-G1 population, early apoptotic cells, and later apoptotic cells. TEDGMA-induced apoptotic mechanisms were found to activate caspase 8, 9, and 3 in OCCM.30 cells, respectively ( P < 0.05). In addition, both c-Jun N-terminal kinase (JNK) inhibitor JNK-in-8 and p38 inhibitor SB203580 dramatically reduced TEGDMA-induced caspase 8, 9, and 3 activations in OCCM.30 cells, respectively ( P < 0.05). Conclusion Taken together, our results demonstrated that TEDGMA decreased cell viability and induced the apoptotic cell death in cementoblast. In addition, caspase-mediated cell apoptosis was found to be associated with JNK and p38 signal transduction pathways.

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