Epigallocatechin-3-gallate blocks triethylene glycol dimethacrylate-induced cyclooxygenase-2 expression by suppressing extracellular signal-regulated kinase in human dental pulp and embryonic palatal mesenchymal cells.

Abstract

INTRODUCTION:

Methacrylate resin-based materials could release components into adjacent environment even after polymerization. The major components leached include triethylene glycol dimethacrylate (TEGDMA). TEGDMA has been shown to induce the expression of cyclooxygenase-2 (COX-2). However, the mechanisms are not completely understood. The aims of this study were to investigate the molecular mechanism underlying TEGDMA-induced COX-2 in 2 oral cell types, the primary culture of human dental pulp (HDP) cells and the human embryonic palatal mesenchymal (HEPM) pre-osteoblasts, and to propose potential strategy to prevent or ameliorate the TEGDMA-induced inflammation in oral tissues.

METHODS:

TEGDMA-induced COX-2 expression and its signaling pathways were assessed by Western blot analyses in HDP and HEPM cells. The inhibition of TEGDMA-induced COX-2 protein expression using various dietary phytochemicals was investigated.

RESULTS:

COX-2 protein expression was increased after exposure to TEGDMA at concentrations as low as 5 μmol/L. TEGDMA-induced COX-2 expression was associated with reaction oxygen species, the extracellular signal-regulated kinase 1/2, and the p38 mitogen-activated protein kinase signaling pathways in HDP and HEPM cells. The activation of p38 mitogen-activated protein kinase was directly associated with reactive oxygen species. Epigallocatechin-3-gallate suppressed TEGDMA-induced COX-2 expression by inhibiting phosphorylation of extracellular signal-regulated kinase 1/2.

CONCLUSIONS:

Cells exposed to low concentrations of TEGDMA may induce inflammatory responses of the adjacent tissues, and this should be taken into consideration during common dental practice. Green tea, which has a long history of safe beverage consumption, may be a useful agent for the prevention or treatment of TEGDMA-induced inflammation in oral tissues.

• Authors: Wan-Hsien Yang, Yi-Ting Deng, Mark Yen-Ping Kuo, Cheing-Meei Liu, Hao-Hueng Chang, Jenny Zwei-Chieng Chang
• Journal: Journal of endodontics (J Endod) Vol. 39 Issue 11 Pg. 1407-12 (Nov 2013) ISSN: 1878-3554 [Electronic] United States
• PMID: 24139263 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2013 American Association of Endodontists. Published by Elsevier Inc. All rights reserved.

Chemical References

• Composite Resins
• Cyclooxygenase 2 Inhibitors
• Polymethacrylic Acids
• Reactive Oxygen Species
• triethylene glycol dimethacrylate
• Polyethylene Glycols
• Catechin
• epigallocatechin gallate
• Cyclooxygenase 2
• PTGS2 protein, human
• Extracellular Signal-Regulated MAP Kinases
• Mitogen-Activated Protein Kinase 1
• Mitogen-Activated Protein Kinase 3
• p38 Mitogen-Activated Protein Kinases

Topics

• Catechin (analogs & derivatives, pharmacology)
• Cell Culture Techniques
• Cell Line
• Cells, Cultured
• Composite Resins (pharmacology)
• Cyclooxygenase 2 (drug effects)
• Cyclooxygenase 2 Inhibitors (pharmacology)
• Dental Pulp (drug effects, enzymology)
• Extracellular Signal-Regulated MAP Kinases (drug effects)
• Humans
• MAP Kinase Signaling System (drug effects)
• Mesenchymal Stem Cells (drug effects, enzymology)
• Mitogen-Activated Protein Kinase 1 (antagonists & inhibitors, drug effects)
• Mitogen-Activated Protein Kinase 3 (antagonists & inhibitors, drug effects)
• Osteoblasts (drug effects, enzymology)
• Palate (cytology)
• Polyethylene Glycols (pharmacology)
• Polymethacrylic Acids (pharmacology)
• Reactive Oxygen Species (metabolism)
• p38 Mitogen-Activated Protein Kinases (antagonists & inhibitors, drug effects)