Davallialactone reduces inflammation and repairs dentinogenesis on glucose oxidase-induced stress in dental pulp cells

J Endod. 2013 Nov;39(11):1401-6. doi: 10.1016/j.joen.2013.06.033. Epub 2013 Sep 6.

Abstract

Introduction: The chronic nature of diabetes mellitus (DM) raises the risk of oral complication diseases. In general, DM causes oxidative stress to organs. This study aimed to evaluate the cellular change of dental pulp cells against glucose oxidative stress by glucose oxidase with a high glucose state. The purpose of this study was to test the antioxidant character of davallialactone and to reduce the pathogenesis of dental pulp cells against glucose oxidative stress.

Methods: The glucose oxidase with a high glucose concentration was tested for hydroxy peroxide (H2O2) production, cellular toxicity, reactive oxygen species (ROS) formation, induction of inflammatory molecules and disturbance of dentin mineralization in human dental pulp cells. The anti-oxidant effect of Davallilactone was investigated to restore dental pulp cells' vitality and dentin mineralization via reduction of H2O2 production, cellular toxicity, ROS formation and inflammatory molecules.

Results: The treatment of glucose oxidase with a high glucose concentration increased H2O2 production, cellular toxicity, and inflammatory molecules and disturbed dentin mineralization by reducing pulp cell activity. However, davallialactone reduced H2O2 production, cellular toxicity, ROS formation, inflammatory molecules, and dentin mineralization disturbances even with a long-term glucose oxidative stress state.

Conclusions: The results of this study imply that the development of oral complications is related to the irreversible damage of dental pulp cells by DM-induced oxidative stress. Davallialactone, a natural antioxidant, may be useful to treat complicated oral disease, representing an improvement for pulp vital therapy.

Keywords: Davallialactone; dental pulp cells; dentin mineralization; diabetes mellitus; glucose oxidase; glucose oxidative stress; inflammation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Agaricales
  • Alkaline Phosphatase / analysis
  • Angiogenic Proteins / analysis
  • Anti-Inflammatory Agents / pharmacology*
  • Antioxidants / pharmacology*
  • Cell Survival / drug effects
  • Cells, Cultured
  • Cytokines / drug effects
  • Dental Pulp / cytology
  • Dental Pulp / drug effects*
  • Dentin / drug effects
  • Dentinogenesis / drug effects*
  • Diabetes Mellitus / metabolism
  • Glucose / metabolism
  • Glucose Oxidase / drug effects*
  • Humans
  • Hydrogen Peroxide / antagonists & inhibitors
  • Hydrogen Peroxide / metabolism
  • Inflammation Mediators / analysis
  • Lactones / pharmacology*
  • Oxidative Stress / drug effects*
  • Plant Extracts / pharmacology
  • Pulpitis / prevention & control*
  • Reactive Oxygen Species / metabolism
  • Tooth Calcification / drug effects

Substances

  • Angiogenic Proteins
  • Anti-Inflammatory Agents
  • Antioxidants
  • Cytokines
  • Inflammation Mediators
  • Lactones
  • Plant Extracts
  • Reactive Oxygen Species
  • davallialactone
  • Hydrogen Peroxide
  • Glucose Oxidase
  • Alkaline Phosphatase
  • Glucose