Evidence map›Paper›PMID 27119009›Full record

ArticleOxidative medicine and cellular longevity2016

The Natural Polyphenol Epigallocatechin Gallate Protects Intervertebral Disc Cells from Oxidative Stress.

Olga Krupkova, Junichi Handa, Marian Hlavna, Juergen Klasen, Caroline Ospelt, Stephen John Ferguson, Karin Wuertz-Kozak

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

51 citing papers in PubMed, 71 citations in OpenAlex.

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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

7 authors at 3 institutions in 3 countries.

Olga KrupkovaDepartment of Health Sciences and Technology, Institute for Biomechanics, ETH Zurich, Hoenggerbergring 64, 8093 Zurich, Switzerland.
Junichi HandaDepartment of Health Sciences and Technology, Institute for Biomechanics, ETH Zurich, Hoenggerbergring 64, 8093 Zurich, Switzerland; Department of Orthopaedic Surgery, Fukushima Medical University School of Medicine, Hikarigaoka, Fukushima City, Fukushima 960-1295, Japan.
Marian HlavnaDepartment of Health Sciences and Technology, Institute for Biomechanics, ETH Zurich, Hoenggerbergring 64, 8093 Zurich, Switzerland.
Juergen KlasenProdorso, Walchestrasse 15, 8006 Zurich, Switzerland.
Caroline OspeltDepartment of Rheumatology, University Hospital, Zurich, Switzerland.
Stephen John FergusonDepartment of Health Sciences and Technology, Institute for Biomechanics, ETH Zurich, Hoenggerbergring 64, 8093 Zurich, Switzerland.
Karin Wuertz-KozakDepartment of Health Sciences and Technology, Institute for Biomechanics, ETH Zurich, Hoenggerbergring 64, 8093 Zurich, Switzerland.
ETH Zurich · CHDepartment of Medical Sciences · BYUniversity Hospital of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress-related phenotypic changes and a decline in the number of viable cells are crucial contributors to intervertebral disc degeneration. The polyphenol epigallocatechin 3-gallate (EGCG) can interfere with painful disc degeneration by reducing inflammation, catabolism, and pain. In this study, we hypothesized that EGCG furthermore protects against senescence and/or cell death, induced by oxidative stress. Sublethal and lethal oxidative stress were induced in primary human intervertebral disc cells with H2O2 (total n = 36). Under sublethal conditions, the effects of EGCG on p53-p21 activation, proliferative capacity, and accumulation of senescence-associated β-galactosidase were tested. Further, the effects of EGCG on mitochondria depolarization and cell viability were analyzed in lethal oxidative stress. The inhibitor LY249002 was applied to investigate the PI3K/Akt pathway. EGCG inhibited accumulation of senescence-associated β-galactosidase but did not affect the loss of proliferative capacity, suggesting that EGCG did not fully neutralize exogenous radicals. Furthermore, EGCG increased the survival of IVD cells in lethal oxidative stress via activation of prosurvival PI3K/Akt and protection of mitochondria. We demonstrated that EGCG not only inhibits inflammation but also can enhance the survival of disc cells in oxidative stress, which makes it a suitable candidate for the development of novel therapies targeting disc degeneration.

Indexed as

AdultAgedAntioxidantsbeta-GalactosidaseCatechinCell DeathCell ProliferationCell SurvivalCellular SenescenceCytoprotectionEnzyme ActivationHumansIntervertebral DiscMembrane Potential, MitochondrialMiddle AgedModels, BiologicalAntioxidantsbeta-GalactosidaseCatechinepigallocatechin gallatePhosphatidylinositol 3-KinasesProtective AgentsProto-Oncogene Proteins c-aktReactive Oxygen Species

Identifiers

PMID27119009
PMCPMC4826942
OpenAlexW2318585930

What OpenQuestion holds

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LicenceCC BY
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.