Urethane dimethacrylate induces cytotoxicity and regulates cyclooxygenase-2, hemeoxygenase and carboxylesterase expression in human dental pulp cells

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• 作者：Hsiao-Hua Chang ; Mei-Chi Chang ; Hsin-Hui Wang ; Guay-Fen Huang ; Yuan-Ling Lee ; Yin-Lin Wang ; Chiu-Po Chan ; Sin-Yuet Yeung ; Shuei-Kuen Tseng ; Jiiang-Huei Jeng
• 关键词：Dental pulp ; Inflammation ; Prostanoids ; Resin monomers ; Urethane dimethacrylate
• 刊名：Acta Biomaterialia
• 出版年：February, 2014
• 年：2014
• 卷：10
• 期：2
• 页码：722-731
• 全文大小：1749 K

文摘

The toxic effect of urethane dimethacrylate (UDMA), a major dental resin monomer, on human dental pulp is not fully clear. In this study, we investigated the influence of UDMA on the cytotoxicity, cell cycle distribution, apoptosis and related gene expression of dental pulp cells. The role of reactive oxygen species, hemeoxygenase-1 (HO-1) and carboxylesterase (CES) in UDMA cytotoxicity, was evaluated. UDMA induced morphological changes of pulp cells and decreased cell viability by 29-49% at concentrations of 0.1-0.35 mM. UDMA induced G0/G1, G2/M cell cycle arrest and apoptosis. The expression of cdc2, cyclinB1 and cdc25C was inhibited by UDMA. Moreover, UDMA stimulated COX-2, HO-1 and CES2 mRNA expression of pulp cells. The cytotoxicity of UDMA was attenuated by N-acetyl-l-cysteine, catalase and esterase, but was enhanced by Zn-protoporphyrin (HO-1 inhibitor), BNPP (CES inhibitor) and loperamide (CES2 inhibitor). Exposure of UDMA may potentially induce the inflammation and toxicity of dental pulp. These findings are important for understanding the clinical response of human pulp to resin monomers after operative restoration and pulp capping, and also provide clues for improvement of dental materials.