The regulation of cytotoxicity and cyclooxygenase-2 expression by 2-hydroxy-ethyl methacrylate in human osteoblasts are related to intracellular glutathione levels

doi:10.1111/iej.12218

中山醫學大學機構典藏 CSMUIR > 口腔醫學院 > 牙醫學系暨碩士班 > 期刊論文 > Item 310902500/18297

Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/18297

Title:	The regulation of cytotoxicity and cyclooxygenase-2 expression by 2-hydroxy-ethyl methacrylate in human osteoblasts are related to intracellular glutathione levels
Authors:	Ho, Y.-C.;Huang, F.-M.;Lee, S.-S.;Chang, Y.-C.
Keywords:	Cyclooxygenase-2;Cytotoxicity;Glutathione;HEMA;Osteoblasts
Date:	2014
Issue Date:	2017-08-14T08:43:43Z (UTC)
Publisher:	Blackwell Publishing Ltd
ISSN:	0143-2885
Abstract:	Aim: 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. © 2013 International Endodontic Journal. Published by John Wiley & Sons Ltd.
URI:	http://dx.doi.org/10.1111/iej.12218 https://www.scopus.com/inward/record.uri?eid=2-s2.0-84903903895&doi=10.1111%2fiej.12218&partnerID=40&md5=dd599f74b4d07d1ab34c37ffb0ab5810 https://ir.csmu.edu.tw:8080/ir/handle/310902500/18297
Relation:	International Endodontic Journal 47 (8) ,784-790
Appears in Collections:	[牙醫學系暨碩士班] 期刊論文

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