Evidence map›Paper›PMID 26489899›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2015

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

Yang Jiao, Sai Ma, Yirong Wang, Jing Li, Lequn Shan, Jihua Chen

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.4field-weighted citation impact, top 19% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Protection against HEMA-Induced Mitochondrial InjuryOxidative medicine and cellular longevity · 2019
    Article
  5. Article
  6. Review
  7. Review
  8. Fabrication and Characterization of Carbon Fiber-Reinforced Nano-Hydroxyapatite/Polyamide46 Biocomposite for Bone Substitute.Medical science monitor : international medical journal of experimental and clinical research · 2017
    Article
  9. Article
  10. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Yang JiaoState Key Laboratory of Military Stomatology, Department of Prosthodontics, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, China (mainland).
Sai MaState Key Laboratory of Military Stomatology, Department of Prosthodontics, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, China (mainland).
Yirong WangShaanxi Key Laboratory of Military Stomatology, Xi'an, Shaanxi, China (mainland).
Jing LiDepartment of Orthopaedic Oncology, Xijing Hospital Affiliated to The Fourth Military Medical University, Xi'an, Shaanxi, China (mainland).
Lequn ShanDepartment of Orthopaedic Surgery, Tangdu Hospital, The Fourth Military Medical University, Xi'an, Shaanxi, China (mainland).
Jihua ChenState Key Laboratory of Military Stomatology, Department of Prosthodontics, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, China (mainland).
Air Force Medical University · CNXijing Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Oxidative StressAnimalsAntioxidantsApoptosisBiocompatible MaterialsCatechinDental PulpDogsGlutathioneMaleMiceMice, KnockoutNF-E2-Related Factor 2Oxidation-ReductionPhenotypeReactive Oxygen SpeciesAntioxidantsBiocompatible MaterialsCatechinepigallocatechin gallateGlutathioneNfe2l2 protein, mouseNF-E2-Related Factor 2Reactive Oxygen SpeciesResins, Synthetic

Identifiers

PMID26489899
PMCPMC4622224
OpenAlexW2155641160

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.