FU-MEI HUANGSHIUAN-SHINN LEEYU-CHAO CHANG2026-10-162026-10-162014-08-01Pure ID: 15383585Pure UUID: 5f986e57-f45e-44f9-ba44-a1d43315a0fb10.1111/iej.12218https://www.scopus.com/pages/publications/84903903895https://scholars.csmu.edu.tw/handle/123456789/27832Aim: To investigate the effects of 2-hydroxy-ethyl methacrylate (HEMA) on cytotoxicity and cyclooxygenase-2 (COX-2) protein expression in human osteoblasts. Methodology: Cytotoxicity was judged using an Alamar Blue reduction assay on human osteoblast cell line U2OS. Western blot was used to evaluate the expression of COX-2 protein by HEMA. To determine whether glutathione (GSH) levels were important in cytotoxicity and COX-2 expression of HEMA, cells were pre-treated with the GSH precursor, 2-oxothiazolidine-4-carboxylic acid (OTZ), to boost thiol levels, or buthionine sulfoximine (BSO) to deplete GSH. Paired Student's t-tests were applied for the statistical analysis of the results. Results: HEMA demonstrated a cytotoxic effect to U2OS cells in a dose-dependent manner (P < 0.05). The 50% inhibition concentration of HEMA was approximately 3 mmol L-1. HEMA was found to induce COX-2 protein expression in U2OS cells (P < 0.05). The addition of OTZ acted as a protective effect on HEMA-induced cytotoxicity and COX-2 expression (P < 0.05). In contrast, the addition of BSO enhanced HEMA-induced cytotoxicity and COX-2 expression (P < 0.05). Conclusion: Taken together, the levels of HEMA that were tested inhibited cell growth on U2OS cells. HEMA has a significant potential for periapical toxicity. The activation of COX-2 protein expression may be one of the mechanisms of HEMA-induced periapical inflammation. These inhibitory effects were associated with intracellular GSH levels.7enjournal article