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Protective effects of non‐thermal plasma on triethylene glycol dimethacrylate‐induced damage in odontoblast‐like MDPC‐23 cells
Author(s) -
Choi Byul Bo ra,
Choi Jeong Hae,
Lee Hyun Young,
Lee HaeJune,
Song Ki Won,
Kim GyooCheon
Publication year - 2021
Publication title -
international endodontic journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.988
H-Index - 119
eISSN - 1365-2591
pISSN - 0143-2885
DOI - 10.1111/iej.13541
Subject(s) - programmed cell death , apoptosis , flow cytometry , chemistry , prostaglandin e2 , cell growth , microbiology and biotechnology , biochemistry , biology , endocrinology
Aim To evaluate whether the use of non‐thermal plasma (NTP) could reduce triethylene glycol dimethacrylate (TEGDMA)‐mediated damage in MDPC‐23 cells. Methodology The effects of NTP and TEGDMA on MDPC‐23 cell proliferation were tested using WST‐1 assays after pretreatment with NTP for 1 min and exposure to TEGDMA. Live/Dead assays were used to visualize cell death. To monitor the effects of NTP and TEGDMA on the cell cycle and apoptotic cell death, flow cytometry was performed. Western blotting was used to assess changes in protein levels mediated by NTP and TEGDMA treatment, and enzyme‐linked immunosorbent assays were performed to evaluate the effects of NTP and TEGDMA on prostaglandin E 2 (PGE 2 ) expression. One‐way analysis of variance and Duncan's post hoc tests were used for statistical analysis. Results NTP treatment effectively protected cells from TEGDMA‐mediated cell damage and blocked TEGDMA‐mediated cell growth inhibition ( p  < .05). NTP appeared to protect cells from death ( p  < .05) and blocked TEGDMA‐mediated apoptotic cell death. Additionally, NTP reduced TEGDMA‐mediated apoptotic activation of poly (ADP) ribose polymerase‐1 and caspase‐3 ( p  < .05). Furthermore, NTP effectively reduced TEGDMA‐mediated expression of cyclooxygenase‐2 and PGE 2 proteins by inhibiting nuclear factor‐κB protein expression ( p  < .05). Conclusions NTP alleviated TEGDMA‐mediated adverse effects by reducing cytotoxicity and inflammatory reactions in cells exposed to TEGDMA.

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