Huang Fu-Mei, Chou Lin Shin-Shen, Chou Ming-Yung, Chang Yu-Chao
Department of Prosthodontics, Oral Medicine Center, Chung Shan Medical University Hospital, Taichung, Taiwan.
J Biomed Mater Res B Appl Biomater. 2005 Aug;74(2):768-73. doi: 10.1002/jbm.b.30283.
Cyclooxygenase-2 (COX-2) is an inducible enzyme believed to be responsible for prostaglandin synthesis at site of inflammation. Recently, the activation of COX-2 expression may be one of the important pathogenesis of root-canal-sealers-induced periapical inflammation. However, little is known about whether chemical interaction can modulate the COX-2 expression and cytotoxicity induced by formaldehyde-containing-ZOE-based root canal sealers. The aim of this study was to investigate the effects of antioxidants such as catalase, superoxide dismutase (SOD), and N-acetyl-L-cysteine (NAC) on N2- and endomethasone-induced COX-2 mRNA gene and cytotoxicity in human osteoblastic cell line U2OS cells. Our data demonstrated that both formaldehyde-containing-ZOE-based root canal sealers were found to induce COX-2 mRNA gene expression in U2OS cells. The addition of glutathione (GSH) precursor NAC led to decrease the induction of COX-2 mRNA gene expression and cytotoxicity by both N2 and Endomethasone (p < 0.05). However, catalase and SOD lacked the ability to prevent cytotoxicity and COX-2 mRNA gene expression induced by N2 and Endomethasone (p > 0.05). The data presented here demonstrated that the activation of COX-2 mRNA gene expression may be one of the pathogenesis of formaldehyde-containing-ZOE-based root-canal-sealers-induced periapical inflammation. In addition, GSH depletion, but not the attack of oxygen free radicals, could be the mechanism for cytotoxicity and COX-2 mRNA gene expression induced by formaldehyde-containing-ZOE-based root canal sealers. NAC appears as a useful agent in protecting cell damage mediated by formaldehyde-containing-ZOE-based root canal sealers.
环氧化酶-2（COX-2）是一种诱导性酶，被认为在炎症部位负责前列腺素的合成。最近，COX-2表达的激活可能是含甲醛的氧化锌丁香酚类根管封闭剂诱导根尖周炎的重要发病机制之一。然而，关于化学相互作用是否能调节含甲醛的氧化锌丁香酚类根管封闭剂诱导的COX-2表达和细胞毒性，目前知之甚少。本研究的目的是探讨过氧化氢酶、超氧化物歧化酶（SOD）和N-乙酰-L-半胱氨酸（NAC）等抗氧化剂对N2和己酸氯地米松诱导人成骨细胞系U2OS细胞中COX-2 mRNA基因及细胞毒性的影响。我们的数据表明，两种含甲醛的氧化锌丁香酚类根管封闭剂均能诱导U2OS细胞中COX-2 mRNA基因表达。添加谷胱甘肽（GSH）前体NAC可导致N2和己酸氯地米松诱导的COX-2 mRNA基因表达和细胞毒性降低（p<0.05）。然而，过氧化氢酶和SOD缺乏预防N2和己酸氯地米松诱导的细胞毒性和COX-2 mRNA基因表达的能力（p>0.05）。此处呈现的数据表明，COX-2 mRNA基因表达的激活可能是含甲醛的氧化锌丁香酚类根管封闭剂诱导根尖周炎的发病机制之一。此外，GSH耗竭而非氧自由基攻击可能是含甲醛的氧化锌丁香酚类根管封闭剂诱导细胞毒性和COX-2 mRNA基因表达的机制。NAC似乎是一种保护含甲醛的氧化锌丁香酚类根管封闭剂介导的细胞损伤的有用试剂。
