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22 October 2015 : Hypothesis  

Epigallocatechin-3-Gallate Reduces Cytotoxic Effects Caused by Dental Monomers: A Hypothesis

Yang JiaoBCDEF, Sai MaAG, Yirong WangEF, Jing LiBCDF, Lequn ShanBG, Jihua ChenAG

DOI: 10.12659/MSM.895628

Med Sci Monit 2015; 21:3197-3202

Abstract

ABSTRACT: Resin monomers from dental composite materials leached due to incomplete polymerization or biodegradation may cause contact allergies and damage dental pulp. The cytotoxicity of dental resin monomers is due to a disturbance of intracellular redox equilibrium, characterized by an overproduction of reactive oxygen species (ROS) and depletion of reduced glutathione (GSH). Oxidative stress caused by dental resin monomers leads to the disturbance of vital cell functions and induction of cell apoptosis in affected cells. The nuclear factor-erythroid 2-related factor 2 (Nrf2) pathway plays a key role in the cellular defense system against oxidative and electrophilic stress. Epigallocatechin-3-gallate (EGCG) can activate the Nrf2 pathway and induce expression of a multitude of antioxidants and phase II enzymes that can restore redox homeostasis. Therefore, here, we tested the hypothesis that EGCG-mediated protection against resin monomer cytotoxicity is mediated by activation of the Nrf2 pathway. This study will help to elucidate the mechanism of resin monomer cytotoxicity and provide information that will be helpful in improving the biocompatibility of dental resin materials.

Keywords: Antioxidants - metabolism, Animals, Biocompatible Materials, Catechin - chemistry, Dental Pulp - drug effects, Dogs, Glutathione - chemistry, Mice, Mice, Knockout, NF-E2-Related Factor 2 - metabolism, Oxidation-Reduction, Oxidative Stress, Phenotype, Reactive Oxygen Species - metabolism, Resins, Synthetic - toxicity, Tooth - drug effects

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Scientific Editor, Medical Science Monitor, International Scientific Information, Inc., Melville, NY, USA

DOI: 10.12659/MSM.935624

Med Sci Monit 2021; 27:e935624

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Medical Science Monitor eISSN: 1643-3750
Medical Science Monitor eISSN: 1643-3750