Reactive oxygen species removal activity of davallialactone reduces lipopolysaccharide-induced pulpal inflammation through inhibition of the extracellular signal-regulated kinase 1/2 and nuclear factor kappa b pathway.

Abstract

INTRODUCTION:

Davallialactone, hispidin analogues derived from the mushroom Inonotus xeranticus, has antioxidant properties. This study examined whether the reactive oxygen species (ROS) removal activity of davallialactone affects the lipopolysaccharide (LPS)-induced anti-inflammatory activity in human dental pulp cells.

METHODS:

The LPS-induced formation of ROS was analyzed by using dichlorofluorescein diacetate with fluorescence-activated cell sorter, and the expression of inflammatory molecules in primary cultured human dental pulp cells was determined by immunoblotting. The inflammatory mechanism of the davallialactone-involved signal pathway was examined by immunoblotting.

RESULTS:

Davallialactone acted as an antioxidant to confirm the elimination of ROS formation and elevation of Cu/Zn superoxide dismutase and Mn superoxide dismutase expression in LPS-induced pulp cells. The antioxidant activity of davallialactone leads to inhibition of LPS-induced inflammation by blocking the extracellular signal-regulated kinase (ERK1/2) and nuclear factor kappa B (NF-κB) pathway, which decreases the expression of inflammatory molecules such as intercellular adhesion molecule-1, vascular cell adhesion molecule-1, matrix metalloproteinase-2, matrix metalloproteinase-9, inducible nitric oxide synthase, and cyclooxygenase-2. The character of davallialactone was more effective in comparison with N-acetylcysteine as the control antioxidant in this study.

CONCLUSIONS:

Davallialactone has antioxidant activity and anti-inflammatory effects in LPS-induced human dental pulp cells through the suppression of ERK1/2 activation followed by blockage of NF-κB translocation from cytosol into nuclear. Therefore, the good anti-inflammatory capacity of davallialactone might be used for oral diseases such as pulpitis and periodontitis.

• Authors: Nan-Hee Lee, Young-Hee Lee, Govinda Bhattari, In-Kyoung Lee, Bong-Sik Yun, Jae-Gyu Jeon, Pyong-Han Hwang, Ho-Keun Yi
• Journal: Journal of endodontics (J Endod) Vol. 37 Issue 4 Pg. 491-5 (Apr 2011) ISSN: 1878-3554 [Electronic] United States
• PMID: 21419296 (Publication Type: Comparative Study, Journal Article)
• Copyright: Copyright © 2011 American Association of Endodontists. Published by Elsevier Inc. All rights reserved.

Chemical References

• Anti-Inflammatory Agents
• Antioxidants
• Cyclooxygenase 2 Inhibitors
• Fluoresceins
• Fluorescent Dyes
• Free Radical Scavengers
• Lactones
• Lipopolysaccharides
• Matrix Metalloproteinase Inhibitors
• NF-kappa B
• Reactive Oxygen Species
• Vascular Cell Adhesion Molecule-1
• Intercellular Adhesion Molecule-1
• davallialactone
• diacetyldichlorofluorescein
• NOS2 protein, human
• Nitric Oxide Synthase Type II
• Cyclooxygenase 2
• PTGS2 protein, human
• Superoxide Dismutase
• MAPK1 protein, human
• Mitogen-Activated Protein Kinase 1
• Mitogen-Activated Protein Kinase 3
• MMP2 protein, human
• Matrix Metalloproteinase 2
• Acetylcysteine

Topics

• Acetylcysteine (pharmacology)
• Anti-Inflammatory Agents (pharmacology)
• Antioxidants (pharmacology)
• Cell Separation
• Cells, Cultured
• Cyclooxygenase 2 (drug effects)
• Cyclooxygenase 2 Inhibitors (pharmacology)
• Dental Pulp (cytology, drug effects)
• Flow Cytometry
• Fluoresceins
• Fluorescent Dyes
• Free Radical Scavengers (pharmacology)
• Humans
• Intercellular Adhesion Molecule-1 (drug effects)
• Lactones (pharmacology)
• Lipopolysaccharides (antagonists & inhibitors, pharmacology)
• Matrix Metalloproteinase 2
• Matrix Metalloproteinase Inhibitors
• Mitogen-Activated Protein Kinase 1 (antagonists & inhibitors)
• Mitogen-Activated Protein Kinase 3 (antagonists & inhibitors)
• NF-kappa B (antagonists & inhibitors)
• Nitric Oxide Synthase Type II (antagonists & inhibitors)
• Pulpitis (pathology)
• Reactive Oxygen Species (antagonists & inhibitors)
• Superoxide Dismutase (drug effects)
• Vascular Cell Adhesion Molecule-1 (drug effects)