Evidence map›Paper›PMID 19445683›Full record

ArticleArthritis research & therapy2009

Green tea polyphenol epigallocatechin-3-gallate inhibits advanced glycation end product-induced expression of tumor necrosis factor-alpha and matrix metalloproteinase-13 in human chondrocytes.

Zafar Rasheed, Arivarasu N Anbazhagan, Nahid Akhtar, Sangeetha Ramamurthy, Frank R Voss, Tariq M Haqqi

Open access · goldAbstract readComparative Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Arthritis research & therapy, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
7.0field-weighted citation impact, top 3% 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

62 citing papers in PubMed, 132 citations in OpenAlex.

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  19. Epigallocatechin-3-Pharmaceutical biology · 2022
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2 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Zafar RasheedDepartment of Pathology, School of Medicine, University of South Carolina, Columbia, SC 29209, USA. zafar.rasheed@uscmed.sc.edu
Arivarasu N Anbazhagan
Nahid Akhtar
Sangeetha Ramamurthy
Frank R Voss
Tariq M Haqqi
University of South Carolina · US

Funding

MECHANISMS OF CHONDROPROTECTION BY POMEGRANATE FRUIT EXTRACTR01AT003627 · NCCIH · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI HAQQI, TARIQ M · 2007 to 2011
$1.7M
NCCIH NIH HHS AT-003267NCCIH NIH HHS R01 AT003627
6 · The paper itself

Abstract

introductionThe major risk factor for osteoarthritis (OA) is aging, but the mechanisms underlying this risk are only partly understood. Age-related accumulation of advanced glycation end products (AGEs) can activate chondrocytes and induce the production of proinflammatory cytokines and matrix metalloproteinases (MMPs). In the present study, we examined the effect of epigallocatechin-3-gallate (EGCG) on AGE-modified-BSA (AGE-BSA)-induced activation and production of TNFalpha and MMP-13 in human OA chondrocytes.

methodsHuman chondrocytes were derived from OA cartilage by enzymatic digestion and stimulated with in vitro-generated AGE-BSA. Gene expression of TNFalpha and MMP-13 was measured by quantitative RT-PCR. TNFalpha protein in culture medium was determined using cytokine-specific ELISA. Western immunoblotting was used to analyze the MMP-13 production in the culture medium, phosphorylation of mitogen-activated protein kinases (MAPKs), and the activation of NF-kappaB. DNA binding activity of NF-kappaB p65 was determined using a highly sensitive and specific ELISA. IkappaB kinase (IKK) activity was determined using an in vitro kinase activity assay. MMP-13 activity in the culture medium was assayed by gelatin zymography.

resultsEGCG significantly decreased AGE-stimulated gene expression and production of TNFalpha and MMP-13 in human chondrocytes. The inhibitory effect of EGCG on the AGE-BSA-induced expression of TNFalpha and MMP-13 was mediated at least in part via suppression of p38-MAPK and JNK activation. In addition, EGCG inhibited the phosphorylating activity of IKKbeta kinase in an in vitro activity assay and EGCG inhibited the AGE-mediated activation and DNA binding activity of NF-kappaB by suppressing the degradation of its inhibitory protein IkappaBalpha in the cytoplasm.

conclusionsThese novel pharmacological actions of EGCG on AGE-BSA-stimulated human OA chondrocytes provide new suggestions that EGCG or EGCG-derived compounds may inhibit cartilage degradation by suppressing AGE-mediated activation and the catabolic response in human chondrocytes.

Indexed as

Matrix Metalloproteinase InhibitorsTeaAgedCatechinCells, CulturedChondrocytesFemaleFlavonoidsGene Expression RegulationGlycation End Products, AdvancedHumansMaleMatrix Metalloproteinase 13Middle AgedPhenolsPolyphenolsadvanced glycation end products-bovine serum albuminCatechinepigallocatechin gallateFlavonoidsGlycation End Products, AdvancedMatrix Metalloproteinase 13Matrix Metalloproteinase InhibitorsPhenolsPolyphenolsProtease InhibitorsSerum Albumin, BovineTeaTumor Necrosis Factor-alpha

Identifiers

PMID19445683
PMCPMC2714117
OpenAlexW2083740873

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.