N-Acetyl cysteine prevents suppression of oral fibroblast function on poly(methylmethacrylate) resin

被引:41
|
作者
Att, Wael [1 ]
Yamada, Masahiro [1 ]
Kojima, Norinaga [1 ]
Ogawa, Takahiro [1 ]
机构
[1] Univ Calif Los Angeles, Sch Dent, Jane & Jerry Weintraub Ctr Reconstruct Biotechnol, Div Adv Prosthodont Biomat & Hosp Dent, Los Angeles, CA 90095 USA
关键词
Dental resin; Bone cement; Cytotoxicity; Fibroblasts; NAC; HUMAN GINGIVAL FIBROBLASTS; CELL-CYCLE ARREST; IN-VITRO; PULP CELLS; GLUTATHIONE CONCENTRATION; MOUSE FIBROBLASTS; APOPTOSIS; CYTOTOXICITY; BONE; COMPONENTS;
D O I
10.1016/j.actbio.2008.07.021
中图分类号
R318 [生物医学工程];
学科分类号
0831 ;
摘要
Despite the proven cytotoxicity, poly(methylmethacrylate) (PMMA) resin is one of the most frequently and extensively used materials in medical and dental fields. The study examined the potential detoxification of the resin material and restoration of the resin-induced suppression of cellular function using an antioxidant amino acid derivative, N-acetyl cysteine (NAC). Oral fibroblasts extracted from rat oral mucosa were cultured on the resin material with or without incorporation of NAC into the material. Twenty-four hour after incubation, less than 2% of the cells were viable on the untreated control resin, while up to 35% of the cells were viable on the resin with incorporation of NAC. At day 7 of culture, the expression of collagen I and III genes was downregulated on the untreated resin, while the cells on NAC-supplemented resin showed the expression levels similar to those in polystyrene culture. The cells produced three times greater amount of collagen on the NAC-supplemented resin than on the untreated resin. The data demonstrated that the cytotoxicity of PMMA resin was substantially lower when the material contains NAC. The potential usefulness of this principle should be explored with a view of developing biocompatible polymer-based materials in a broad range of dental and medical resin materials and tissue engineering scaffolds. (C) 2008 Acta Materialia Inc. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:391 / 398
页数:8
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